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Review

From Lasers to Longevity: Exploring Energy-Based Devices as Senotherapeutic Tools in Dermatology

by
Oana Mihaela Condurache Hrițcu
1,
Victor-Vlad Costan
1,
Ștefan Vasile Toader
2,*,
Daciana Elena Brănișteanu
3 and
Mihaela Paula Toader
1
1
Department of Surgicals, Faculty of Dental Medicine, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, Romania
2
Department of Physiopathology, Faculty of Dental Medicine, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, Romania
3
Department of Dermatology, Faculty of Medicine, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, Romania
*
Author to whom correspondence should be addressed.
Cosmetics 2025, 12(5), 201; https://doi.org/10.3390/cosmetics12050201
Submission received: 13 August 2025 / Revised: 9 September 2025 / Accepted: 10 September 2025 / Published: 15 September 2025
(This article belongs to the Special Issue Feature Papers in Cosmetics in 2025)
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Abstract

Background: Cutaneous aging is a multifactorial process, increasingly understood through the lens of cellular senescence, a state of stable cell cycle arrest accompanied by a pro-inflammatory secretory phenotype that disrupts tissue homeostasis. Recent research has highlighted the accumulation of senescent dermal fibroblasts as a key contributor to age-related skin changes, including loss of elasticity, collagen degradation, and impaired regeneration. Objective: This review explores the emerging hypothesis that energy-based devices (EBDs), particularly lasers, may act as senotherapeutic tools by targeting cellular senescence pathways in aging skin. We examine the molecular and histological effects of laser therapy in relation to known biomarkers of senescence and evaluate their potential role in regenerative dermatology. Methods: We conducted a review of published studies on fractional lasers, red-light therapies, and other EBDs, focusing on their impact on fibroblast activity, extracellular matrix remodeling, and senescence-associated markers such as p16INK4a, p21Cip1, telomerase, and SASP-related cytokines. Comparative analysis with pharmacologic senotherapeutics was also performed. Results: Preclinical and clinical data suggest that specific EBDs can modulate dermal aging at the molecular level by enhancing mitochondrial activity, increasing type III collagen synthesis, reducing senescence-related gene expression, and promoting fibroblast turnover. In contrast to systemic senolytics, lasers provide localized and titratable interventions with a favorable safety profile. Conclusions: Energy-based devices, particularly fractional lasers and red-light systems, hold promise as non-invasive senotherapeutic interventions in dermatology. By modulating senescence-associated pathways, EBDs may offer not only cosmetic improvement but also biological rejuvenation. Further mechanistic studies and biomarker-based trials are warranted to validate this paradigm and refine treatment protocols for longevity-oriented skin therapies.

1. Introduction

Skin aging is a complex, multifactorial process involving cumulative genetic, environmental, and hormonal influences. In recent years, cellular senescence has emerged as a central driver of cutaneous aging, shifting the paradigm from mere structural degradation to one centered on molecular dysfunction. Senescent cells—particularly dermal fibroblasts—accumulate with age and adopt a senescence-associated secretory phenotype (SASP), characterized by the release of pro-inflammatory cytokines, matrix metalloproteinases (MMPs), and reactive oxygen species (ROS) [1,2,3]. This secretome disrupts normal extracellular matrix (ECM) remodeling, impairs epidermal–dermal communication, and fosters a pro-degenerative microenvironment, ultimately contributing to wrinkling, laxity, and dermal atrophy [4]. Senotherapeutics—a class of interventions aimed at delaying, preventing, or reversing age-related tissue dysfunction by selectively eliminating senescent cells (senolytics) or suppressing their deleterious secretory profile (senomorphics)—have emerged as a promising strategy to counteract these processes [5].
While the aesthetic consequences of skin aging have long been addressed using energy-based devices (EBDs)—such as fractional lasers, intense pulsed light (IPL), radiofrequency (RF), and high-intensity focused ultrasound (HIFU)—these technologies are increasingly recognized for their regenerative potential beyond superficial cosmetic outcomes [6]. Fractional photothermolysis, in particular, induces a controlled pattern of dermal injury that stimulates fibroblast proliferation, neocollagenesis, and angiogenesis [7].
We propose a novel hypothesis: certain EBDs may function as “senotherapeutic” agents, capable of remodeling, suppressing, or even clearing senescent fibroblasts in the skin. By activating regenerative pathways, modulating SASP components, and enhancing ECM integrity, lasers and related devices may offer not only cosmetic rejuvenation but also biological reversal of age-associated dermal decline (Figure 1).
Senotherapeutics encompass a rapidly growing class of interventions designed to mitigate the detrimental effects of cellular senescence. By definition, they either selectively eliminate senescent cells (senolytics) or suppress the senescence-associated secretory phenotype (SASP) without killing the cells (senomorphics). Senolytic strategies typically exploit vulnerabilities of senescent cells, such as their reliance on anti-apoptotic pathways, by targeting proteins from the BCL-2 family, the PI3K/AKT signaling cascade, or modulating stress response axes controlled by p53/p21Cip1 and p16INK4a/Rb. In contrast, senomorphics attenuate the chronic inflammatory and degradative profile of senescent cells through the inhibition of NF-κB, mTOR and other transcriptional regulators of the SASP.
In cutaneous tissues, these mechanisms converge primarily on dermal fibroblasts and keratinocytes, two major cellular populations that accumulate senescent features with age and chronic UV exposure. Senescent fibroblasts exhibit diminished collagen synthesis and enhanced production of matrix metalloproteinases, driving extracellular matrix breakdown, while keratinocyte senescence impairs epidermal renewal and barrier integrity. Together, they create a pro-inflammatory milieu characterized by chronic low-grade inflammation (“inflammaging”), oxidative stress, and impaired tissue remodeling.
Understanding these mechanistic foundations is essential for contextualizing how energy-based devices (EBDs) may act as localized senotherapeutic tools. By inducing controlled microinjury, stimulating immune-mediated clearance, and promoting regenerative signaling, lasers and related modalities may remodel the senescent niche, restore extracellular matrix homeostasis, and enhance functional cell turnover. This positions EBDs as potential non-pharmacological strategies to complement or even substitute systemic senotherapies in dermatologic practice [8].
The aims of this article are threefold: to review the current understanding of cutaneous senescence, with a focus on fibroblast biology and the molecular mediators of skin aging; to analyze the effects of energy-based devices—particularly lasers—on senescence-associated markers and pathways, drawing from in vitro, in vivo, and clinical studies; and to propose a conceptual model for “laser senotherapy,” framing EBDs as localized, non-invasive tools within the broader field of regenerative and longevity-oriented dermatology.

2. Materials and Methods

This article is a narrative review that synthesizes current evidence on the potential role of energy-based devices (EBDs) as senotherapeutic agents in dermatology. The methodology involved a literature search, critical appraisal, and thematic synthesis of findings from both preclinical and clinical studies.

2.1. Search Strategy and Selection Criteria

We systematically searched PubMed, Scopus, and Web of Science for energy-based device (EBD) studies published between January 2020 and July 2025. The strategy combined controlled vocabulary and free-text terms, including “skin aging,” “cellular senescence,” “senotherapeutics,” “energy-based devices,” “fractional laser,” “radiofrequency,” “HIFU,” “photobiomodulation,” “SASP,” and “fibroblast senescence.” Only English-language records were considered. Eligible articles were reviews and original investigations—in vitro, ex vivo, in vivo, or clinical studies evaluating EBD effects on senescence markers (e.g., p16INK4a, p21Cip1, and SA-β-gal), SASP components, or regenerative endpoints (e.g., collagen synthesis and fibroblast activity). We excluded non-dermatologic EBD applications and studies without senescence- or regeneration-related outcomes. Review articles were consulted to contextualize senotherapeutics and broader mechanisms. To situate the EBD evidence within the field, we also drew on the non-EBD literature regarding skin senescence and senotherapeutics (2010–2025).

2.2. Data Extraction and Thematic Analysis

Data were extracted regarding EBD type, mechanism of action, study design, biomarkers assessed, and reported effects on senescence. A thematic synthesis was performed, grouping results under mechanistic hypotheses, evidence tiers (in vitro, animal, and clinical), and therapeutic implications. Emphasis was placed on identifying potential senolytic or senomorphic roles of EBDs and on differentiating them from pharmacologic approaches.

3. Results

Out of 61 papers on EBDs identified based on the search terms, 16 were excluded after screening for relevance and duplication. We further analyzed 45 eligible papers, including clinical (15) and preclinical (3) studies, as well as 27 review papers. A summary of the included clinical and preclinical studies assessing senescence-related skin outcomes after EBD treatment is presented in Table 1. An additional 72 papers regarding cutaneous senescence and senotherapeutics were also consulted.

3.1. Skin Senescence: Molecular and Clinical Landscape

The skin, as the body’s largest organ, is uniquely vulnerable to both intrinsic (chronologic) and extrinsic (environmental) aging influences. Among the most significant biological processes driving cutaneous aging is cellular senescence, a state of durable cell cycle arrest that occurs in response to stressors such as telomere shortening, oxidative damage, ultraviolet (UV) radiation, and genotoxic insults [27,28,29].

3.1.1. Mechanisms of Cellular Senescence in the Skin

Senescent cells remain metabolically active but no longer proliferate, and they undergo marked alterations in gene expression and function. The accumulation of these cells in the skin, particularly among dermal fibroblasts, has been implicated in key features of skin aging such as collagen loss, matrix disorganization, epidermal thinning, and impaired wound healing [30,31,32]. Molecular hallmarks of senescence include the upregulation of cyclin-dependent kinase inhibitors, notably p16INK4a and p21Cip1, which enforce irreversible growth arrest via the p53/p21 and p16/Rb pathways [33,34]; secretion of the senescence-associated secretory phenotype (SASP), a bioactive milieu of pro-inflammatory cytokines (e.g., IL-6 and IL-8), matrix metalloproteinases (MMP-1 and MMP-3), and reactive oxygen species (ROS) that perpetuate tissue inflammation and ECM degradation [35,36,37]; and telomere attrition and epigenetic remodeling, further contributing to genomic instability and altered cellular function [38,39].

3.1.2. Clinical Consequences of Dermal Senescence

The dermal compartment is particularly sensitive to senescence-driven degradation. Senescent fibroblasts produce less type I and III collagen, secrete MMPs that degrade the existing matrix, and show diminished responsiveness to pro-regenerative signals such as TGF-β and PDGF [40,41]. This results in skin laxity and atrophy, fine lines and wrinkles, delayed wound healing, and decreased dermal vascularization. Moreover, the paracrine effects of SASP factors can propagate senescence to neighboring cells (termed bystander senescence), amplifying tissue dysfunction and accelerating visible aging [42,43]. Emerging research also suggests that senescent cell burden in the skin is predictive of overall biological age, making it a potential biomarker for systemic aging and longevity [44,45]. Selective removal of p16INK4a-positive cells in animal models has been associated with improved dermal elasticity and reduced inflammation [46].

3.2. Energy-Based Devices in Dermatology

Energy-based devices (EBDs) have revolutionized aesthetic dermatology by providing non-invasive methods to improve skin texture, tone, elasticity, and pigmentation. Traditionally employed for photorejuvenation, scar remodeling, and pigmentary correction, these technologies are now being re-evaluated for their potential to modulate dermal biology at the cellular level [47,48].

3.2.1. Classification and Mechanisms of Action

EBDs encompass a diverse group of technologies that deliver thermal or mechanical energy to target tissues in a controlled manner. The main classes include the following:
  • Ablative lasers (e.g., CO2 at 10,600 nm and Er:YAG at 2940 nm): remove epidermis and induce coagulative dermal damage, stimulating intense neocollagenesis and resurfacing [49,50];
  • Non-ablative fractional lasers (e.g., 1550 nm Er: Glass and 1927 nm Thulium): create dermal microthermal zones (MTZs) while sparing the epidermis, enabling controlled wound healing with minimal downtime [51];
  • Pulsed dye lasers (PDL) and Nd:YAG lasers: primarily for vascular lesions but also capable of dermal remodeling [52];
  • Low-level light therapy (LLLT) and photobiomodulation (e.g., red light 675 nm or green light 532 nm): modulate mitochondrial activity and cellular signaling without significant thermal injury [53,54];
  • Radiofrequency (RF) and microneedling RF: generate deep dermal heating via electromagnetic waves, stimulating fibroblast activity and ECM regeneration [9,10,13,23,55];
  • High-intensity focused ultrasound (HIFU): delivers ultrasound energy to the SMAS and deep dermis, inducing collagen denaturation and neocollagenesis [56].
Device parameters—such as wavelength, fluence, pulse duration, and density—determine penetration depth, target chromophore, and biostimulatory potential, allowing treatments to be tailored to specific clinical goals [57,58]. (Table 2)

3.2.2. Biological Effects of EBD Treatment Relevant to Senescence

Beyond cosmetic outcomes, multiple EBDs have demonstrated molecular and histologic changes consistent with regenerative remodeling: increased collagen types I and III production [59,60,61]; fibroblast proliferation and migration [62]; upregulation of growth factors such as TGF-β, VEGF, and FGF-2 [63]; angiogenesis and improved dermal vascularity [64]; and reduction in MMP expression, balancing ECM synthesis and degradation [65,66].
Fractional microneedle RF improved rejuvenation outcomes and modulated the senescent fibroblast niche more effectively than microneedling [9,10], while non-ablative fractional diode lasers and picosecond alexandrite systems demonstrated senomorphic remodeling effects [11,12,13,14]. Microblade RF and innovative CO2 scanning technologies yielded clinical improvements in skin texture and treatment efficiency [13,15]. CO2 fractional lasers in human fibroblast and UVB-mouse models reduced SA-β-gal activity, increased collagen I/III, and upregulated SOD and SMAD3 [15,26,67]. Multiple laser modalities have been reviewed as potent inducers of neocollagenesis and ECM remodeling [68]. Ablative and non-ablative Er:YAG lasers in human trials showed histologic increases in collagen I/III and fibroblast activation [24,25,69]. Green-light photobiomodulation reduced SA-β-gal and MMP-1 while increasing collagen and autophagy in UVB-damaged fibroblasts [18,70]. Importantly, the MTZs created by fractional devices trigger a controlled wound-healing cascade that may facilitate clearance or suppression of senescent cells, aligning with the concept of laser senotherapy [11,12,14,21,22,71,72].

3.2.3. Safety, Precision, and Adaptability

EBDs offer a localized, titratable therapeutic approach, allowing got precise modulation of tissue injury and remodeling. This minimizes systemic side effects and enables safe use across a wide range of skin phototypes [73,74]. Advances in delivery systems and fractional scanning patterns have improved reproducibility, safety, and treatment customization [32].

3.2.4. Senotherapeutic Effects of EBD Treatments

Given the emerging data on the interaction between energy-based devices (EBDs) and cellular senescence, it is increasingly relevant to explore how such technologies may exert senotherapeutic effects beyond cosmetic outcomes. Preclinical and clinical studies have reported changes in senescence markers, mitochondrial activity, and extracellular matrix (ECM) dynamics following laser and light-based interventions [75,76].
In Vitro and Ex Vivo Studies
Multiple in vitro and ex vivo models have shed light on the regenerative and anti-senescent effects of EBDs. In vitro and animal models highlighted the potential of OLED and red/green-light photobiomodulation to reverse senescent phenotypes and enhance collagen synthesis [16,17,18,19]. Red-light laser at 675 nm stimulated fibroblast proliferation, increased type III collagen, and enhanced mitochondrial respiration, with downregulation of p16INK4a and activation of TGF-β signaling [19,77]. Fractional non-ablative Er: Glass lasers (1550 nm) applied to 3D skin equivalents upregulated COL1A1 and elastin (ELN) genes while reducing SA-β-gal activity [24,25,78]. Photobiomodulation in red and near-infrared ranges activated cytochrome c oxidase, increased ATP production, reduced oxidative stress, and suppressed senescence-inducing pathways [79,80]. Green-light photobiomodulation decreased SA-β-gal, increased collagen I/III, reduced MMP-1, and promoted autophagy in UVB-exposed fibroblasts [81].
Animal and Clinical Studies
In vivo evidence supports the hypothesis that certain EBDs can remodel or suppress senescent cell populations. HIFU promoted ECM regeneration by downregulating senescence-associated pathways [20]. Additional studies confirmed that non-ablative and picosecond Nd:YAG lasers, as well as fractional Er:YAG and CO2 lasers, consistently enhanced collagen production, fibroblast activation, and reduced senescence markers [21,22,23,24,25,26]. The use of an ablative fractional CO2 laser in aged murine skin restored collagen density and reduced MMP-9 and IL-6, both SASP components [82]. Fractional CO2 laser resurfacing in aged human skin biopsies showed reduced p16INK4a and increased telomerase reverse transcriptase (TERT) expression [83]. Microneedling RF demonstrated histologic improvement in dermal architecture and reduction in SASP cytokines in treated areas [9,10,13,23,84]. Er:YAG resurfacing improved wrinkles and texture with histologic evidence of fibroblast activation and new collagen deposition [24,25,85].
Limitations of Current Evidence
Despite encouraging findings, important limitations exist:
  • Lack of standardized biomarkers: Many studies rely on collagen quantification or wrinkle scoring rather than direct senescence markers [86].
  • Short follow-up periods: Persistence of anti-senescent effects remains uncertain [87].
  • Limited human biopsy data: More clinical trials with serial biopsies are needed, particularly in older populations [88].

3.3. Comparison with Pharmacologic Senotherapeutics

The concept of senotherapy has gained traction in recent years as researchers target senescent cells to mitigate age-related degeneration. While pharmacologic approaches—including senolytics (agents that selectively clear senescent cells) and senomorphics (agents that suppress the SASP)—have demonstrated promising results in systemic aging models, their application to dermatology remains largely theoretical. In contrast, EBDs offer a localized, non-systemic, and physically controlled alternative to these pharmacologic strategies [89].

3.3.1. Pharmacologic Senotherapeutics: Mechanisms and Limitations

Senotherapeutics are classified into two main categories: senolytics, which induce apoptosis selectively in senescent cells by inhibiting pro-survival pathways (e.g., BCL-2 and PI3K/AKT) [8,90], and senomorphics, which suppress SASP-related pathways (e.g., mTOR and NF-κB) [91,92]. Examples of pharmacologic senolytics include Dasatinib + Quercetin, Navitoclax, and Fisetin. Several challenges related to these treatments are the possible off-target effects, systemic toxicity (e.g., thrombocytopenia with Navitoclax), and poor skin penetration when used topically. Examples of pharmacologic senomorphics include Rapamycin, Metformin, and Curcumin. However, they require chronic administration, have limited ability to reverse structural changes, and act by modulation rather than clearance of senescent cells (Table 3).

3.3.2. EBDs as Localized Senotherapeutic Agents

Compared to drug-based approaches, lasers and EBDs offer several distinct advantages for skin-specific applications [93,94,95]: they induce a controlled injury leading to regeneration and remodeling, promoting neocollagenesis and structural recovery, and they are highly selective, with minimal side effects, as established by clinical studies (Table 3). EBDs may not eliminate senescent cells directly, but they offer a multi-layered therapeutic effect—functional remodeling, suppression of SASP, and enhanced dermal regeneration—making them ideal candidates for cutaneous senotherapy [96,97].

3.3.3. Synergistic Potential

The future may lie in combination approaches, for instance, using fractional lasers to enhance skin permeability and delivery of topical senolytics or pairing red-light therapy with low-dose metabolic modulators to enhance mitochondrial rejuvenation. Such hybrid regimens could amplify outcomes while minimizing drug doses and systemic risks [98]. In addition, recent evidence highlights the potential of sequential ablative and non-ablative fractional lasers. A narrative review on combined fractional CO2 with 1540/1570 nm non-ablative wavelengths demonstrated synergistic benefits in both preclinical and clinical settings, supporting enhanced neocollagenesis, dermal remodeling, and safety profiles when modalities are combined [99]. This further reinforces the concept that multimodal laser strategies may represent a promising avenue for senotherapeutic interventions.

4. Discussion

4.1. Mechanistic Hypotheses: How Lasers May Target Senescence

Although direct senolytic effects of energy-based devices (EBDs) have not yet been definitively demonstrated, several plausible mechanisms suggest that lasers and related technologies may modulate or reverse cellular senescence in skin tissue. These effects appear to result from a combination of controlled injury, immune activation, mitochondrial modulation, and microenvironmental remodeling, which together facilitate the clearance, suppression, or functional reprogramming of senescent cells [82,83], (Figure 2).

4.2. Future Directions and Clinical Implications

The concept of “laser senotherapy” is at the intersection of aesthetic dermatology and regenerative science. While existing evidence suggests that EBDs can modulate key aspects of dermal senescence, the field is still in its early stages [100]. Most studies assessing EBD efficacy rely on subjective endpoints: clinical appearance, wrinkle scores, or patient satisfaction. To truly validate the senotherapeutic potential of lasers, future trials must include serial skin biopsies pre- and post-treatment, quantification of senescence-associated markers (e.g., p16INK4a, p21Cip1, SA-β-gal, and TERT), measurement of SASP components (IL-6, IL-8, and MMP-1), and imaging technologies (e.g., RCM and multiphoton microscopy) for non-invasive biomarker tracking [101,102,103,104].
Given the diversity of skin types and aging patterns, there is a need to develop personalized treatment protocols based on the stratification of patients according to the senescence burden or biological skin age, tailoring of laser fluence, density, and modality to optimize regenerative over destructive effects, and the incorporation of combination therapies where appropriate.
Importantly, skin phenotype—including Fitzpatrick phototype, baseline pigmentation, vascularity, sebaceous activity, and intrinsic versus extrinsic aging patterns—exerts a strong influence on both the safety and the effectiveness of EBD interventions. For example, darker skin phototypes (IV–VI) have a greater predisposition to post-inflammatory hyperpigmentation and dyschromia after ablative or high-energy procedures, while lighter phototypes (I–II) may exhibit more pronounced vascular reactivity and erythema. Similarly, atrophic, thin skin with reduced dermal reserves is more vulnerable to scarring, delayed wound healing, or prolonged erythema, whereas thicker, sebaceous-rich skin may demonstrate greater resilience but less visible remodeling after treatment.
Other variables—such as chronologic versus photoinduced aging, hormonal status, and the presence of coexisting dermatologic conditions (e.g., melasma, rosacea, and chronic actinic damage)—further modulate tissue response to energy-based interventions. Integrating these factors into treatment planning, whether through risk stratification models, biometric assessment tools (e.g., imaging-based quantification of dermal thickness or senescent cell markers), or phenotype-specific guidelines, could significantly enhance both safety and efficacy.
Thus, the future of laser senotherapy lies not only in mechanistic validation but also in the framework of precision dermatology, where protocols are tailored to individual skin biology, aging trajectory, and risk profile. Such a patient-centered approach could maximize rejuvenative outcomes, minimize complications, and align laser interventions with broader goals of extending cutaneous health span [103,104].
While current EBDs are mostly used for cosmetic rejuvenation, their senotherapeutic properties could extend their applications to chronic wounds and ulcers (where senescence impairs healing), radiation-induced skin damage, postmenopausal dermal atrophy, and photoaged skin in high-UV-exposed populations [105].
There are several ethical and safety considerations, as positioning lasers as senotherapeutic agents also demands long-term safety data (especially with repeated treatments), regulatory clarity on claims related to “anti-aging” or “cellular rejuvenation”, and avoidance of over-treatment in the pursuit of biomarker modification without clinical benefit [106].
Our research has several limitations that should be acknowledged. As a narrative review, this article does not involve quantitative meta-analysis. The findings are subject to publication bias and variability in study protocols. Future work should include standardized clinical trials with longitudinal biomarker tracking to substantiate the proposed hypotheses [107,108,109,110,111,112].

5. Conclusions

The emerging concept of laser senotherapy challenges the traditional boundaries of aesthetic dermatology, proposing that EBDs—particularly fractional lasers and red-light systems—may not only rejuvenate the skin’s appearance but also remodel its biological age [113]. Through mechanisms involving microinjury-induced regeneration, SASP suppression, mitochondrial activation, and growth factor modulation, EBDs hold potential to reduce senescent cell burden and restore tissue function [114,115].
While pharmacologic senotherapeutics have dominated the anti-aging discourse in systemic medicine, their application to the skin remains limited by safety, penetration, and regulatory concerns. In contrast, lasers provide a localized, titratable, and clinically established modality with a growing body of evidence suggesting benefits beyond cosmetic enhancement. To fully validate this paradigm, biomarker-driven studies are essential, linking clinical outcomes with changes in molecular markers of senescence. Furthermore, integrating precision treatment protocols, longitudinal biometrics, and multi-modal approaches may help usher in a new era of preventive and regenerative dermatology, where laser therapies are recognized not only as tools of beauty but also as instruments of cutaneous health span extension [116,117].

Author Contributions

Conceptualization, O.M.C.H. and M.P.T.; methodology, O.M.C.H.; validation, D.E.B.; formal analysis, V.-V.C. and Ș.V.T.; investigation, O.M.C.H.; resources, V.-V.C., Ș.V.T. and D.E.B.; data curation, D.E.B. and M.P.T.; writing—original draft preparation, O.M.C.H.; writing—review and editing, M.P.T.; visualization, V.-V.C., Ș.V.T. and D.E.B.; supervision, M.P.T. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

The original data presented in the study are openly available. All resources are stated in the “References” section.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
EBDsEnergy-based devices
SASPSenescence-associated secretory phenotype
MMPsMatrix metalloproteinases
ECMExtracellular matrix
IPLIntense pulsed light
RFRadiofrequency
HIFUHigh-intensity focused ultrasound
UVUltraviolet
MTZsDermal microthermal zones
LLLTLow-level light therapy
ROSReactive oxygen species
EMElectromagnetic radiation

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Figure 1. Conceptual framework of EBD-induced senotherapeutic effects on dermal aging through clearance of senescent cells, SASP modulation and ECM remodeling.
Figure 1. Conceptual framework of EBD-induced senotherapeutic effects on dermal aging through clearance of senescent cells, SASP modulation and ECM remodeling.
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Figure 2. Conceptual framework illustrating mechanistic pathways through which lasers may influence senescent cell clearance, SASP suppression, and dermal regeneration.
Figure 2. Conceptual framework illustrating mechanistic pathways through which lasers may influence senescent cell clearance, SASP suppression, and dermal regeneration.
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Table 1. Summary of energy-based device studies assessing senescence-related skin outcomes.
Table 1. Summary of energy-based device studies assessing senescence-related skin outcomes.
YearStudyEBD TypeDevice/ParamsModel/PopulationDesignEvidence TagBiomarkersEffect on Senescence/SASPReference
2025Sci Rep: FMR with topical antioxidant serum for neckFractional microneedle RFFMR + antioxidant serumHuman clinical (neck skin)Clinicalclinical (human)Clinical + histologyEnhanced rejuvenation outcomes vs. FMR alone[9]
2025Fractional microneedle RF vs. microneedling on senescent milieuFractional microneedle RFFMRF vs. MNHuman aged skinClinical + molecularclinical (human)Senescent fibroblast milieu markersFMRF modulated senescent fibroblast niche; superior to MN[10]
2025Non-ablative fractional 1940-nm diode laser for rejuvenationNAFL (1940 nm)1940 nm diodeHuman clinicalClinicalclinical (human)Clinical outcomes; superficial thermal remodelingImproved superficial remodeling; supports senomorphic effect[11]
2025Activated melanocytes and senescent collagen fibers—PAL DLA protocolPicosecond alexandrite (DLA)755 nm; DLA; 3 sessionsHuman clinical (protocol)Protocol/clinicalclinical (human)Optical markers; collagenTargets senescent collagen fibers; remodeling[12]
2025Pilot: microblade RF for neck rejuvenationMicroblade RFDual lengthHuman clinical (neck)Pilot clinicalclinical (human)Skin properties; wrinklesClinical improvement; remodeling[13]
2024Picosecond 755 nm DLA laser for wrinkles (clinical)Picosecond alexandrite (DLA)755 nm; diffractive lens arrayHuman clinical (wrinkles)Prospective clinicalclinical (human)Clinical wrinkle scales; histology subsetImproved wrinkles; supports photomechanical remodeling[14]
2024A faster CO2 fractional scanner mode for full-face rejuvenationCO2 fractional laserScanner “moveo” vs. standardHuman clinicalClinical performanceclinical (human)Treatment time; clinical outcomesImproved efficiency; remodeling effects implied[15]
2024OLED therapy reduces aging signs; stem-cell senescence recoveryOLED PBMOLED panelCell/animalPreclinicalin vitroStem cell senescenceRecovery from senescence[16]
2023Photomodulation alleviates cellular senescence of aging ASCsPhotobiomodulation (LED)Light activation at P3Human adipose-derived stem cellsIn vitroin vitrop16, p21, p53↓ p16/p21/p53 in aged cells[17]
2023Green-light pretreatment reduces SA-β-Gal (clinical context)Green-light PBMLow-energy green lightIn vitro + concept to clinicPreclinicalclinical (human)SA-β-gal, collagen I/III, MMP-1↓ SA-β-gal; ↑ collagen[18]
2023Reverse skin aging signs by red-light PBM (clinical)Photobiomodulation (red LED 630 ± 10 nm)15.6 J/cm2; 12 min; 2×/week; 3 monthsHuman clinical (facial skin)Prospective clinicalclinical (human)Clinical: elasticity, texture; (mechanistic narrative)Improved clinical aging signs; consistent with PBM-induced mitochondrial benefits[19]
2023HIFU increases collagen/elastin via Cav-1 modulationHIFU0.5 J LINEAR modeSenescent fibroblasts + aging skin modelIn vitro + in vivoin vivo + in vitroAc-p53, p21, cyclin D1, PCNA; collagen/elastin↓ p53/p21; ↑ proliferation markers; ↑ collagen/elastin[20]
2023Non-ablative lasers offer a gentle approach (news + study refs)Non-ablative fractional lasersNAFL vs. MFRHuman clinicalClinical (summarized)clinical (human)Clinical laxity, wrinklesImproved remodeling; indirect senomorphic effect[21]
2021Picosecond Nd:YAG (532/1064) improves photoaged skinPicosecond Nd:YAG532/1064 nmHuman clinical/ex vivoClinical/ex vivoex vivoCollagen III increasePhotomechanical remodeling[22]
2021Synergistic effect of 300 μm FMR needle depth on pigmentationFractional microneedle RF300 μm needle depthHuman clinical (pigmentation disorders)Clinical observationalclinical (human)Basement membrane markers; keratinocyte senescence contextSuggests removal of senescent keratinocytes; repairs BM[23]
2020Microneedling vs. fractional Er:YAG for rejuvenationFractional Er:YAGEr:YAG fractional; microneedling comparatorHuman clinicalClinical comparativeclinical (human)Clinical scores; histology subsetImproved wrinkles
/texture; suggests remodeling		[24]
2020Non-ablative vs. ablative Er:YAG fractional resurfacingEr:YAG (ablative and NAFL)Er:YAG fractionalHuman clinicalClinical comparativeclinical (human)Collagen I/III (histology), fibroblast markers↑ Collagen I/III; fibroblast activation[25]
2020CO2 lattice laser reverses UVB-induced skin agingCO2 fractional laserCO2 lattice; UVB photoaging modelHuman fibroblasts + UVB-micein vitro + in vivoin vivo + in vitroSA-β-gal, collagen I/III, SOD, SMAD3↓ SA-β-gal; ↑ collagen; antioxidant upregulation[26]
Table 2. Characteristics of common energy-based devices used in skin rejuvenation.
Table 2. Characteristics of common energy-based devices used in skin rejuvenation.
Device TypeWavelength/ModalityPenetration Depth/TargetChromophore/TargetMechanism of ActionClinical IndicationsKey Features/Notes
Ablative CO2 Laser10,600 nmEpidermis + dermisWaterVaporizes tissue → stimulates neocollagenesisWrinkles, scars, and deep resurfacingGold standard for deep rejuvenation
Ablative Er:YAG Laser2940 nmEpidermisWaterPrecise ablation → collagen remodelingFine wrinkles and superficial scarsHigh precision and minimal thermal damage
Non-Ablative Fractional Lasers1550 nm/1927 nmDermal MTZWaterMicrothermal injury → repair responseRejuvenation, downtime reductionDeep remodeling and low downtime
Pulsed Dye Lasers (PDLs)~585–595 nmSuperficial dermisHemoglobinVascular targeting → stimulates remodelingVascular lesions and rejuvenationMultifaceted impact
Intense Pulsed Light (IPL)Broad 400–1200 nmVariableMelanin and hemoglobinBroad-spectrum light → chromophore absorptionPigmentation and photorejuvenationVersatile but less specific
Radiofrequency (RF) (monopolar/tri-/microneedling)Non-ionizing EMDeep dermisWater and collagen frameworksThermal heating → neocollagenesisTightening and collagen inductionSafe for all skin types and minimal pigment risk
High-Intensity Focused Ultrasound (HIFU)Ultrasound energySMAS + deep dermisAcoustic focusThermal coagulation → collagen remodelingSkin lifting and tighteningDeep-targeting and non-invasive
Light-Emitting Diodes (LEDs and LLLT)600–1100 nm (e.g., 660 nm)Mitochondrial levelCytochrome c oxidasePhotobiomodulation → improves ATP and reduces ROSBiostimulation and mild rejuvenationNon-thermal and low risk
Table 3. Comparison of pharmacologic senotherapeutics and energy-based devices.
Table 3. Comparison of pharmacologic senotherapeutics and energy-based devices.
ParameterPharmacologic SenotherapeuticsEnergy-Based Devices (EBDs)
DeliverySystemic or topical (limited skin penetration)Localized and operator controlled
MechanismMolecular inhibition or apoptosisControlled injury → regeneration/remodeling
SelectivityPathway dependentTissue compartment specific
Onset of ActionDelayed (weeks to months)Immediate to short term
Side EffectsSystemic toxicity and off-target effectsMinimal with appropriate parameters
Evidence in SkinMostly preclinicalClinical studies available
Reversibility of ECM damageLimitedPromotes neocollagenesis and structural recovery
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Hrițcu, O.M.C.; Costan, V.-V.; Toader, Ș.V.; Brănișteanu, D.E.; Toader, M.P. From Lasers to Longevity: Exploring Energy-Based Devices as Senotherapeutic Tools in Dermatology. Cosmetics 2025, 12, 201. https://doi.org/10.3390/cosmetics12050201

AMA Style

Hrițcu OMC, Costan V-V, Toader ȘV, Brănișteanu DE, Toader MP. From Lasers to Longevity: Exploring Energy-Based Devices as Senotherapeutic Tools in Dermatology. Cosmetics. 2025; 12(5):201. https://doi.org/10.3390/cosmetics12050201

Chicago/Turabian Style

Hrițcu, Oana Mihaela Condurache, Victor-Vlad Costan, Ștefan Vasile Toader, Daciana Elena Brănișteanu, and Mihaela Paula Toader. 2025. "From Lasers to Longevity: Exploring Energy-Based Devices as Senotherapeutic Tools in Dermatology" Cosmetics 12, no. 5: 201. https://doi.org/10.3390/cosmetics12050201

APA Style

Hrițcu, O. M. C., Costan, V.-V., Toader, Ș. V., Brănișteanu, D. E., & Toader, M. P. (2025). From Lasers to Longevity: Exploring Energy-Based Devices as Senotherapeutic Tools in Dermatology. Cosmetics, 12(5), 201. https://doi.org/10.3390/cosmetics12050201

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