Search Results (301)

Hair follicle homeostasis is influenced by hormonal pathways, the scalp microenvironment, and environmental stressors such as pollution, UV radiation, and oxidative stress. Elissara^®, a polyphenol-enriched botanical ingredient, has shown benefits for scalp moisturization, barrier function, sebum regulation, and redness. Building on these scalp-level benefits, we investigated Elissara’s effects on follicular signaling, survival-associated biomarkers, oxidative damage, and androgen-related pathways as potential contributors to follicular health, using in silico, in vitro, and ex vivo models. Molecular docking (AutoDock Vina) of the main Elissara bioactives (oleuropein, hydroxytyrosol, verbascoside, carnosic acid, carnosol, and quercetin) identified SRD5A2 as a favorable predicted target, with individual binding energies ranging from −8.70 to −9.73 kcal/mol, approaching finasteride/dutasteride reference values. As an exploratory approach, simultaneous multi-ligand docking showed favorable global docking outputs for several targets, indicating that multiple bioactives could be structurally accommodated within complementary regions of the binding site. In human follicle dermal papilla cells, Elissara significantly increased BrdU incorporation to 245.70% of control at 0.002% and reduced SRD5A2 protein levels by 18.48% at 0.006%. In human scalp explants, Elissara at 200 µg/mL increased β-catenin, Bcl-2, and collagen IV under basal conditions and counteracted acute PM_2.5/UVA-induced alterations in β-catenin, Ki67-positive cells, Bcl-2, IGF-1, collagen IV, and protein carbonylation. Together, these findings support the potential of Elissara as a promising nutricosmetic ingredient for supporting follicular resilience through multiple follicle-relevant pathways. Clinical studies assessing hair growth outcomes are needed to determine whether these preclinical findings translate into measurable benefits. Full article

Oxidative stress contributes to hair follicle aging, melanocyte dysfunction, and androgen-related hair disorders, yet chemically characterized botanical interventions with multi-target activities remain incompletely defined. This study evaluated the antioxidant, follicle-supporting, and antiandrogenic potential of Eucommia ulmoides bark extract (EUE) using integrated in vitro and in vivo approaches and characterized EUE by HPLC-DAD using geniposidic acid and chlorogenic acid as representative marker compounds. Chlorogenic acid and geniposidic acid were present at 3.21 ± 0.01 and 1.88 ± 0.15 mg/g extract, respectively. In replicate-well assays using H₂O₂-challenged B16 melanoma cells, EUE increased superoxide dismutase activity and reduced malondialdehyde accumulation. Technical-triplicate RT-qPCR measurements and a single Western blot experiment showed descriptive changes in Nrf2 and HO-1 markers; these observations are exploratory and require independent biological replication. In HDPCs, replicate-well viability assays and technical-triplicate RT-qPCR measurements indicated concentration-associated viability changes and descriptive changes in VEGF, Wnt5a, and β-catenin transcripts. EUE also inhibited 5α-reductase activity in a cell-free assay, although the non-monotonic response and the much higher mass concentrations used relative to finasteride preclude potency equivalence. In male C57BL/6 mice, topical EUE attenuated H₂O₂-induced suppression of hair follicle elongation and improved follicular morphology. Overall, EUE is a chemically characterized botanical extract with preliminary biological activities relevant to oxidative stress- and androgen-associated hair disorders; independent replication, active-compound identification, marker-specific permeation, and protein-level validation of the measured markers remain necessary. Full article

Background: Noise-induced hearing loss (NIHL) is a pervasive occupational health challenge, yet the individual susceptibility mechanisms remain unclear. Ferroptosis, an iron-dependent form of programmed cell death, has been implicated in cochlear hair cell damage. This study aims to elucidate the regulatory role of the transcription factor FOXA2 and the deacetylase SIRT1 in ferroptosis and to investigate the association between SIRT1 genetic polymorphisms and NIHL susceptibility in occupational populations. Methods: We employed a multi-level study design combining epidemiological investigation, animal models, and cellular experiments. First, a case–control study was conducted involving 1314 noise-exposed workers (639 cases vs. 675 controls) from a chemical fiber enterprise in Jiangsu Province to analyze the association between SIRT1 single nucleotide polymorphisms (SNPs) and NIHL risk. Second, a C57BL/6J mouse model exposed to 120 dB white noise was established to assess cochlear morphology and protein expression. Third, in HEI-OC1 cochlear hair cells, we performed siRNA-mediated knockdown of Foxa2 and dual-luciferase reporter assays to verify the transcriptional regulation of SIRT1 and its downstream effects on the ferroptosis pathway. Results: Population analysis revealed that the SIRT1 rs12778366 C allele was significantly associated with increased NIHL risk (OR = 1.386, 95% CI: 1.084–1.772, p = 0.009), and this association remained significant after adjustment (p = 0.041). Stratified analysis further revealed a significant gene–environment interaction in workers with >15 years of noise exposure (OR = 2.126, 95% CI: 1.401–3.226, p < 0.001). In vivo, noise exposure led to significant downregulation of Sirt1 and Foxa2 in cochlear tissues, accompanied by elevated ferroptosis markers (Fe²⁺, MDA) and depleted antioxidant defenses (GSH, xCT, and GPX4). Mechanistically, we demonstrate that FOXA2 transcriptionally activates SIRT1 by binding to its promoter. Knockdown of FOXA2 in vitro suppressed SIRT1 expression, suppressed xCT, a key component of the System Xc⁻/GPX4 antioxidant axis, and promoted ferroptosis-related cellular changes. Conclusions: This study identifies a novel protective axis where FOXA2 prevents noise-induced ferroptosis in cochlear hair cells by transcriptionally upregulating SIRT1 and maintaining xCT-mediated antioxidant defense. Furthermore, the SIRT1 rs12778366 polymorphism is identified as a candidate variant warranting further investigation in independent cohorts before clinical translation. Full article

Human pigmentation is a quantitative, tissue-specific, and temporally variable phenotype shaped by melanocyte biology, melanosome physiology, regulatory variation, environmental exposure, and population history. This narrative review examines how functional and population-based evidence supports—or limits—the translation of pigmentation genetics into forensic DNA phenotyping (FDP) and health-related applications. A structured search of MEDLINE/PubMed and Google Scholar was conducted through July 2026, prioritizing primary functional studies, independent validations, meta-analyses, and consensus documents. Current evidence supports polygenic and regulatory control of skin, hair, and iris pigmentation, but heterogeneous phenotype definitions, population composition, age, and environmental modulation constrain direct genotype-to-appearance inference. IrisPlex, HIrisPlex, and HIrisPlex-S provide validated probabilistic predictions for selected pigmentation categories; performance is less consistent for intermediate phenotypes, admixed populations, partial profiles, and settings lacking appropriate calibration. Associations with ultraviolet damage and cutaneous cancer are substantial but differ by cancer type, whereas evidence concerning vitamin D, melanin–drug interactions, and broader precision-medicine applications remains context-dependent or preliminary. Progress will require standardized phenotyping, globally representative datasets, transparent uncertainty reporting, and independent forensic and clinical validation. Full article

Ischemia plays a critical role in the pathogenesis of sensorineural hearing loss through the induction of severe cochlear apoptosis and mitochondrial dysfunction. Exosomes derived from adipose-derived mesenchymal stem cells (ADMSC-Exo) have robust protective effects under non-otologic ischemic conditions. However, their otoprotective effects remain unclear. This study aimed to investigate the protective effects of human ADMSC-Exo against cochlear damage and mitochondrial dysfunction under oxygen–glucose deprivation (OGD), an in vitro and ex vivo model of cochlear ischemia. ADMSC-Exo attenuated OGD-induced cytotoxicity and apoptosis in HEI-OC1 cells and reduced the OGD-induced loss of cochlear hair cells in the organ of Corti explants. OGD caused a decrease in mitochondrial mass and mitochondrial membrane potential depolarization and impaired mitochondrial respiration in auditory cells. ADMSC-Exo preserved mitochondrial integrity and improved mitochondrial bioenergetic function following OGD exposure. These effects were accompanied by increased LC3-II conversion and formation of autolysosome-like structures and elevated expression of PINK1 and Parkin, indicating the activation of autophagy and mitophagy-related protective mechanisms. Importantly, 3-methyladenine, an autophagy inhibitor, attenuated the cytoprotective effect of ADMSC-Exo, supporting the involvement of autophagy in ADMSC-Exo-mediated protection. Collectively, these findings suggest that ADMSC-Exo protect against OGD-induced cochlear injury by promoting autophagy-associated mitochondrial protection. Full article

Hair loss is closely associated with oxidative stress, which impairs the function of human follicle dermal papilla cells (HFDPCs) and disrupts hair follicle homeostasis. Current pharmacological treatments, such as minoxidil and finasteride, are effective but may cause adverse effects, highlighting the need for safer alternatives. In this study, we utilized a patented high-pressure processing method to produce black ginseng concentrate (BGC), which is significantly enriched with rare bioactive ginsenosides, including Rg3, Rg5, and Rk1, through optimized chemical transformation. We aimed to elucidate the protective effects of BGC against oxidative stress-induced damage in HFDPCs. BGC significantly reduced intracellular reactive oxygen species (ROS) levels. BGC also improved mitochondrial function, including an increased oxygen consumption rate (OCR). In addition, BGC activated hair growth-related signaling pathways by upregulating Wnt/β-catenin and increasing the phosphorylation levels of ERK and AKT. Collectively, these findings demonstrate that BGC protects HFDPCs from oxidative stress, improves mitochondrial function, and supports key signaling pathways associated with hair growth. This study suggests that BGC has potential as a natural agent for preventing oxidative stress-induced cellular dysfunction related to hair loss. Full article

Cisplatin is a widely used platinum-based chemotherapeutic agent that often causes irreversible hair cell loss, leading to hearing impairment. To date, effective strategies for preventing cisplatin-induced ototoxicity remain limited. Corchorus olitorius L. (COL) is rich in bioactive phytochemicals with antioxidant and anti-inflammatory properties; however, the protective role of COL stem against cisplatin-induced hearing loss has not been explored. This study aimed to determine whether COL stem extract treatment could mitigate cisplatin-induced hair cell damage in the lateral line system of zebrafish. Herein, we use 7-day post-fertilization (dpf) transgenic zebrafish larvae as a high-throughput screening platform to assessed COL stem extract against cisplatin-induced hair cell injury. Endpoints included mechanotransduction (MET) function, reactive oxygen species (ROS) production, apoptotic and inflammatory responses, and locomotor behavior. Antioxidant capacity and acute toxicity were also evaluated. Pretreatment with COL stem extract preserved hair cell viability, restored MET function, reduced ROS accumulation, upregulated Nrf-2-dependent cytoprotective genes, suppressed apoptosis, and attenuated macrophage infiltration. The recovery of swimming behavior correlated with hair cell protection, confirming the phenotypic relevance. This study demonstrates, for the first time, that COL stem exerts potent otoprotective effects through antioxidative, anti-apoptotic, and anti-inflammatory mechanisms, contributes to maintain mechanosensory function and swimming behavior. The findings support COL stem as a promising candidate for otoprotection and validate zebrafish-based high-throughput screening for novel therapeutic discovery. Full article

The interfacial behavior of hybrid nanoparticles on biological substrates governs their functional performance. Here, we investigate how surface properties and colloidal stability dictate the pH-dependent adhesion of oxybenzone-loaded palygorskite nanohybrids to hair—a model biological interface. A series of hybrids with 5–50% oxybenzone loadings were prepared via melt impregnation. XRD and FTIR analyses confirm hydrogen bonding between oxybenzone and palygorskite, forming stable organic–inorganic hybrids. The colloidal stability of these nanohybrids varies non-monotonically with oxybenzone loading, governed by surface hydrophilicity and zeta potential, exhibiting a network-like behavior upon pH change. Optimal stability is achieved at an intermediate loading with a favorable balance of surface properties. While pristine hybrids show no affinity for hair, surface modification with cationic polyquaternium-7 (PQ-7) or non-ionic polyvinylpyrrolidone (PVP) enables effective deposition through distinct pH-dependent mechanisms: PQ-7 operates optimally at pH 10 via electrostatic attraction, whereas PVP performs best at pH 4 through hydrogen bonding, forming a protective coating layer on the hair surface. Deposition fails for PVP-modified hybrids at 50% loading due to excessive surface hydrophobicity. The deposited hybrids provide exceptional UV protection, significantly mitigating cuticle damage, suppressing photo-yellowing, and minimizing protein oxidation. Among the hybrids, hybrid-35 exhibited the best colloidal stability, whereas PQ-7-modified hybrid-50 gave the highest UV protection (color difference ΔE reduced from 10.51 to 1.60). The adhesion rates of the two best-performing hybrids were 2.70% and 2.85%, respectively. Beyond hair protection, we evaluate the environmental interface of these materials. While free oxybenzone is highly toxic to Chlorella vulgaris, hybridization drastically reduces its ecotoxicity. Remarkably, palygorskite and the hybrids promote algal growth, likely by acting as nutrient adsorbents and attachment sites. This work provides fundamental insights into particle–biointerface interactions and offers a strategy for designing functional hybrid materials with tailored surface properties for bio-related applications. Full article

Nanoplastics from plastic waste degradation pose a growing environmental health risk, yet size-dependent dermal effects remain poorly understood. This study investigated polystyrene nanoplastics of 50, 100, and 200 nm using ex vivo porcine skin and in vitro human keratinocyte models. Skin permeation, cellular uptake, viability, oxidative stress, inflammation, autophagy, and transcriptomic pathways were assessed. Enhanced nanoparticle penetration was observed in barrier-disrupted skin, primarily via hair follicles, with smaller particles showing greater intracellular accumulation. Transcriptomics revealed disruptions in oxidative stress, inflammation, endocytosis, and autophagy pathways. Specifically, 50 nm particles induced the strongest oxidative stress via Nrf2 activation and triggered sustained autophagy, leading to proliferation inhibition and time-dependent inflammation. In contrast, 100 nm particles caused moderate oxidative and inflammatory effects, whereas 200 nm particles provoked acute cytotoxicity, pronounced endocytosis, and an early inflammatory burst with subdued autophagy. These findings demonstrate that sub-100 nm PS NPs exhibit enhanced skin penetration in barrier-disrupted ex vivo models and induce pronounced oxidative stress, sustained autophagy, and proliferation inhibition in human keratinocytes. While these results suggest potential cellular mechanisms that may contribute to dermal toxicity, they do not directly demonstrate systemic absorption or long-term damage in vivo. Our observations provide a mechanistic basis for future in vivo investigations and highlight the need for caution when extrapolating in vitro findings to human health risks. Full article

Hair follicle (HF) stem cells are multipotent adult stem cells that play a key role in the hair follicle cycle. However, it remains poorly understood how the outer root sheath (ORS)—specifically, the stem cells in the bulge region of the hair follicle—promotes skin repair. This study aims to investigate the role of bulge stem cells in tissue growth and repair and to determine whether the ORS of transplanted hair follicles can facilitate skin repair. We further seek to elucidate the mechanisms by which bulge stem cells contribute to hair follicle development, regeneration, and skin wound healing. In this study, hair follicle samples were obtained from neonatal mice using microdissection. Hair follicle morphology was assessed by Sirius red staining, H&E staining, and transmission electron microscopy. Immunofluorescence staining was used to detect changes in CD34 and SOX9 protein expression. Additionally, microdissection-based hair follicle transplantation and Western blotting were employed to investigate protein activation and inhibition in the Wnt/β-catenin signaling pathway. The results show that the hair follicle bulge, inner root sheath, and dermal papilla all increase in size as hair follicles grow, with each structure growing relatively rapidly on day 7. Treatment with Teplinovivint effectively inhibits the expression of Wnt/β-catenin signaling pathway-related proteins and hair follicle stem cell markers. Damaged hair follicle tissues cultured in vitro are capable of self-repair. At the transplantation site, the skin gradually closes as the outer root sheath wound heals. In contrast, the central region of the outer root sheath becomes progressively filled with numerous dividing cells and extracellular matrix. The inner portion of the outer root sheath is densely populated with cells, and the markers CD34 and SOX9 are also widely distributed. This indicates that activation of the Wnt/β-catenin signaling pathway enhances the proliferation and differentiation of hair follicle stem cells, thereby promoting hair follicle growth, repair of damaged follicles, and healing of skin wounds. Furthermore, this study demonstrates the feasibility of using transplanted outer root sheath (ORS) to repair skin wounds—specifically, the potential to achieve large-scale hair regeneration from a limited number of hair follicle stem cells—providing a new approach for the clinical treatment of skin injury disorders. Nevertheless, achieving long-term, stable, and scalable clinical translation of ORS stem cells for hair follicle regeneration remains a major challenge. Full article

Background: Sensorineural hearing loss (SNHL) is increasingly recognized as a disorder involving not only hair-cell damage but also selective degeneration of spiral ganglion neurons (SGNs). Recent single-cell, molecular, and functional studies have refined the classical type I/type II classification of SGNs by identifying distinct Ia, Ib, and Ic subtypes within type I neurons. This review aims to synthesize current evidence on how SGN vulnerability is shaped by the interaction between subtype identity, life stage, and injury context. Methods: We conducted a critical narrative review of recent studies on SGN heterogeneity and subtype-specific vulnerability across development, maturity, and aging, with particular attention to molecular profiling, functional studies, and emerging therapeutic strategies. Results: SGN degeneration in SNHL is not uniform. During development, the available evidence mainly supports the vulnerability of subtype specification, synaptogenesis, and activity-dependent maturation, rather than direct selective degeneration of mature Ia/Ib/Ic identities. In the mature cochlea, subtype-specific differences in synaptic architecture, ion-channel composition, and metabolic demand appear to shape responses to noise, ototoxic drugs, and ischemic stress, with Ic-related populations often showing greater vulnerability. During aging, cumulative mitochondrial dysfunction, oxidative stress, chronic inflammation, and declining neurotrophic support may progressively unmask differences in subtype resilience and contribute to age-related auditory decline. Conclusions: A lifespan-oriented and subtype-informed framework may improve the current understanding of selective SGN degeneration and support the development of more precise neuroprotective and reparative strategies for SNHL. Full article

Mutations in gap junction protein β-2 (GJB2), encoding Connexin 26 (Cx26), are the most common genetic cause of hearing loss, responsible for up to 50% of inherited non-syndromic cases worldwide. This review covers Cx26 from three perspectives: protein structure, mutant disease mechanisms, and treatment approaches. Structurally, 12 Cx26 subunits assemble into a gap junction channel connecting neighboring cells, enabling exchange of ions and signaling molecules; activity is regulated by calcium, pH, and CO₂. In the cochlea, Cx26 channels are required for the development of sound-sensing hair cells, maintenance of the electrical gradient needed for hearing, and energy supply during sound processing. GJB2 mutations cause hearing loss through three mechanisms, complete loss of functional protein, failure of channel assembly or membrane delivery, and abnormal channel gating, that damage cochlear cells. Severity ranges from profound congenital deafness to gradual decline, depending on which mutations are inherited. Gene therapy, genome editing, and pharmacological approaches are under investigation; cochlear implantation remains the current standard of care. Full article

Consumer demand for sustainable solutions to protect against hair damage is growing, yet quantitative studies linking molecular interactions to mechanical strengthening and structural changes remain limited. Here, we investigated the effectiveness of biotechnologically obtained Saccharomyces Lysate as a formulated active ingredient for hair care. Molecular modeling was used to explore the interactions between peptides in the lysate and keratin and suggested a network of intermolecular interactions at multiple sites on the proteins. Based on these observations, the strength and structural integrity of hair fibers treated with Saccharomyces Lysate were assessed using tensile measurements. We observed an improvement in the strength of bleached hair tresses, with an increased Young’s modulus compared to tresses treated only with water along with a significantly increased break stress. To visualize the hair fibers and their surface roughness after treatment with the lysate, we employed micro-computed tomography (µ-CT) offering high-resolution visualization of hair fibers. We introduce this method to qualitatively highlight surface appearance following application of a cosmetic product and complemented it with combing force measurements. Our results demonstrate the potential of this complex mixture of small peptides to strengthen hair integrity and we propose a hypothesis for its putative mode of action at the molecular level. Full article

Chemotherapy-induced alopecia (CIA) is a distressing side effect of cancer treatment with limited effective therapeutic options. While CIA has traditionally been attributed to direct p53-mediated cytotoxicity against rapidly proliferating keratinocytes in hair bulbs, emerging evidence suggests a more complex pathogenesis that involves immune-mediated mechanisms analogous to those in alopecia areata (AA). This review synthesizes current literature and proposes that CIA may be fundamentally driven by the collapse of hair follicle (HF) immune privilege (IP). We explore how chemotherapy-induced DNA damage and psychophysiological stress converge to trigger inflammation, characterized by interferon-γ (IFN-γ)-driven pathways, oxidative stress, and neuroimmune dysregulation. We highlight histopathological, genetic, and clinical overlaps between CIA and AA, particularly regarding the shared involvement of the Janus Kinase-Signal Transducer and Activator of Transcription (JAK-STAT) signaling pathway. Consequently, Janus kinase (JAK) inhibitors (JAKi) are evaluated as potential therapeutic agents for CIA. However, the application of JAKi in oncologic populations requires scrutiny regarding potential immunosuppression and risks of malignancies. Finally, we discuss the context-dependent roles of cytokines involved in the HF-IP collapse pathway, such as interleukin (IL)-15 and IL-1, in HF homeostasis versus inflammation, and we outline future research directions for targeted and safe therapeutic strategies that mitigate CIA without compromising cancer treatment outcomes. Full article

The taxane family of compounds, including paclitaxel, docetaxel (Taxotere), and cabazitaxel (Jevtana), are common drugs used in chemotherapy for the frontline treatment of most major types of cancer. Alopecia, the dramatic loss of hair, is a common side effect that became a symbol of the suffering of many cancer patients. Concerted efforts have been made to understand the mechanism of taxane toxicity to hair follicles and, thus, prevention methods. Taxanes act by stabilizing cellular microtubules, which consequently cause mitotic arrest and then failure, as microtubules play critical functions in chromosome segregation. Hair follicle matrix cells are highly proliferative and thus are exceedingly sensitive to taxanes. We review the cellular mechanism-based strategies under investigation to counter taxane-induced hair follicle damage. These include the application of cyclin kinase inhibitors to block mitotic entry, the practical method using scalp cooling to reduce exposure of scalp hair follicles to drugs during infusion, the requirement of p53 action for hair follicle damage, and the recently discovered method of using low-intensity ultrasound to break taxane-stabilized microtubules and thus reverse taxane toxicity in hair follicle matrix cells. The concept of low-intensity ultrasound as an antidote to taxanes may have the potential to provide a practical and compelling strategy to counter alopecia in cancer treatment using taxanes. Tweet: Taxanes (paclitaxel/docetaxel) are powerful microtubule-stabilizing cancer drugs, but they also cause adverse effects, including alopecia. New research discoveries of temporary microtubule disruption by low-intensity ultrasound may counteract taxane toxicity and prevent alopecia during cancer chemotherapy. “Mechanistic-based strategies for the prevention of taxane-induced hair follicle damage in cancer chemotherapy” OUTLINE: 1. Taxane/paclitaxel mechanism of action in cancer therapy. 2. Taxane side effects: Alopecia (hair loss). 3. p53 dependence of taxane-induced hair follicle damage. 4. Research efforts to counter taxane -induced alopecia by CDK4/6i. 5. Prevention of taxane chemotherapy side effects using scalp cooling. 6. Discovery of low-intensity ultrasound as an antidote for taxane cytotoxicity, and potential prevention of alopecia in chemotherapy using taxanes. 7. Summary and prospective. Full article