Search Results (1,993)

Background and Objective: Romosozumab carries a warning for potential severe cardiovascular events, while denosumab is widely used for osteoporosis but requires safety considerations in advanced chronic kidney disease (CKD). Given the limited direct real-world evidence comparing these treatments, in this study, we aimed to compare the cardiovascular and survival outcomes associated with romosozumab versus denosumab in adults with CKD. Materials and Methods: In this retrospective propensity score-matched cohort study, we utilized de-identified electronic health records from the TriNetX Global Collaborative Network, where eligible participants were adults aged 40 to 90 years with CKD who initiated either romosozumab or denosumab. Patients with bone/bone marrow malignancies or recent acute cardiovascular events were excluded. Following 1:1 propensity score matching based on demographics, diagnoses, medications, and laboratory characteristics, patients were followed for up to 1095 days. The primary outcome was a composite cardiovascular measure (all-cause mortality, acute myocardial infarction, or cerebrovascular event), while secondary outcomes included the individual components of the composite outcome and acute heart failure. Outcomes were evaluated using fixed-window cumulative risks, risk ratios (RRs), odds ratios, and hazard-ratio estimates. Results: After 1:1 propensity score matching, 1201 patients remained in each cohort; the mean age was 74.1 years in the romosozumab cohort and 74.2 years in the denosumab cohort, and 94.9% and 93.8%, respectively, were women. Romosozumab was associated with lower 1095-day cumulative risk of the composite cardiovascular outcome than denosumab (12.6% vs. 18.8%; RR, 0.668 [95% CI, 0.553–0.808]), as well as lower cumulative risk of cerebrovascular event (5.0% vs. 7.0%; RR, 0.714 [95% CI, 0.518–0.985]), all-cause mortality (6.6% vs. 9.5%; RR, 0.693 [95% CI, 0.526–0.913]), acute myocardial infarction (3.8% vs. 6.2%; RR, 0.613 [95% CI, 0.429–0.878]), and heart failure (2.7% vs. 6.1%; RR, 0.438 [95% CI, 0.292–0.659]). Conclusions: In this propensity score-matched EHR cohort of adults with CKD, cardiovascular and survival estimates associated with romosozumab versus denosumab varied by follow-up window and analytic approach. Although 1095-day fixed-window cumulative risks were lower in the romosozumab cohort, corresponding time-to-event estimates were neutral or directionally inconsistent. These findings should not be interpreted as evidence of cardioprotection or causal superiority but rather as showing no clear and consistent excess cardiovascular risk signal for romosozumab compared with denosumab. Full article

Hypertension or high blood pressure drives structural and functional cardiac remodelling through sustained pressure overload, oxidative stress, and chronic inflammation. Lifestyle modifications including regular exercise and a healthy diet including fruits and vegetables help in attenuating high blood pressure. Berries are small fruits abundant in polyphenols, vitamins and minerals which provide these fruits with antioxidant and anti-inflammatory properties. One such berry is the Saskatoon berry (Amelanchier alnifolia), which is rich in anthocyanins and procyanidins with demonstrated cardiometabolic activity, yet its effects on hypertension and cardiac remodelling have not been studied. This study evaluated the impact of 16-week Saskatoon berry supplementation on cardiovascular structure, function, inflammation, and oxidative stress in spontaneously hypertensive rats (SHRs). Age-matched Wistar Kyoto (WKY) rats served as normotensive controls. Saskatoon berry supplementation did not significantly lower systolic or diastolic blood pressure in SHRs; however, echocardiography results revealed trends towards attenuation of hypertensive cardiac remodelling. Saskatoon berry supplementation reduced interventricular septal and posterior wall thickness, decreased left ventricular (LV) mass, and partially preserved systolic function, as reflected by improved ejection fraction and fractional shortening. Diastolic relaxation (IVRT) remained impaired, indicating selective effects on systolic rather than lusitropic function. Serum TNF-α and TBARS were not significantly altered, whereas IL-10 was partially restored, suggesting a modest improvement in systemic inflammatory balance. Principal component analysis integrating all hemodynamic, echocardiographic, and biochemical variables revealed a dominant pathological remodelling axis that distinguished WKY from SHRs. Saskatoon berry supplementation shifted SHRs toward an intermediate multivariate phenotype, supporting a coordinated improvement across structural and functional domains despite persistent hypertension. Together, these findings indicate that Saskatoon berry exerts blood pressure-independent cardioprotective effects that mitigate hypertensive LV hypertrophy and preserve systolic performance. Saskatoon berry may represent a promising functional food ingredient for attenuating cardiac remodelling in hypertension. Full article

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have rapidly evolved from glucose-lowering agents to central players in cardiovascular risk reduction. Evidence from landmark randomized controlled trials has established their capacity to reduce major adverse cardiovascular events, promote anti-inflammatory signaling, attenuate ischemia–reperfusion injury, and improve myocardial metabolic efficiency. As the prevalence of obesity, type 2 diabetes mellitus, and heart failure in the cardiac surgical population grows, GLP-1 RAs are increasingly encountered in the perioperative setting. Yet the cardiac surgery literature has yet to synthesize their emergent role coherently. This is a narrative review; no systematic review or meta-analysis was performed. This narrative review integrates mechanistic, clinical, and translational evidence to reframe GLP-1 RAs as potential perioperative cardioprotective agents in patients undergoing cardiac surgery. We examine receptor-level biology, evidence from the GLOBE randomized trial, observational data linking GLP-1 RA use to reduced postoperative atrial fibrillation after coronary artery bypass grafting, the rationale for the forthcoming REVERSE-TAVR trial, and evolving perioperative management guidelines. Key evidence gaps are identified, including the absence of prospective data in open cardiac surgery, aortic surgery, and high-acuity populations. We propose a research agenda and conceptual framework to guide future investigation into GLP-1 RAs as a new dimension of perioperative cardioprotection. The current evidence is hypothesis-generating; a definitive perioperative cardioprotective benefit has not yet been demonstrated in cardiac surgery populations, and these agents are presented here as potential rather than proven cardioprotective tools. Full article

Apple pomace is an abundant agro-industrial by-product rich in bioactive compounds. In the present study, amphiphilic bioactives from organic Greek Starking and Granny Smith apple pomace were recovered using a green extraction methodology, in compliance with EU legislations for food-grade solvents utilized in food stuffs, followed by evaporation of these solvents in vacuum conditions by flash rotary evaporation. The green extracts were then evaluated for their content in amphiphilic bioactives, as well as for their antioxidant photoprotective capacities spectrophotometrically, and for anti-inflammatory and potential in vitro antithrombotic activities by inhibiting human platelets’ aggregation. ATR-FTIR analysis revealed the presence of phenolics, carotenoids and polar lipids in these extracts. Thus, the total phenolic content (TPC) and total carotenoid content (TCC) were determined spectrophotometrically, while LC–MS analysis facilitated the characterization of specific polar lipid bioactives and quantified their fatty acid composition. Granny Smith extracts exhibited a higher phenolic content and enhanced anti-inflammatory and anti-platelet activities, likely associated with their polar lipid composition and low balanced ω6/ω3 fatty acid ratio, aligned with anti-inflammatory phenolic bioactives that are present in apple pomace. The observed inhibition of platelet aggregation, particularly via the PAF-related inflammatory pathways, suggests potential cardioprotective applications. Moreover, both extracts demonstrated potent antioxidant capacity by all the three mechanisms of action and UV photoprotective properties, probably due to the presence of both phenolic and carotenoid bioactives, with Starking showing stronger UVB-related activity and Granny Smith enhanced UVA-related protection, which—if combined with the observed potent antioxidant capacity and anti-PAF anti-inflammatory properties—further suggest potential applications in functional photoprotective and anti-aging cosmetic formulations. These findings highlight that apple pomace offers a sustainable source of amphiphilic bioactives suitable for nutraceutical and cosmetic applications. Full article

Background: Cisplatin-induced cardiotoxicity is associated with oxidative stress, inflammation, and apoptosis; however, the role of CD38-Sirt3 signaling remains unclear. This study investigated whether apigenin protects against cisplatin-induced cardiac injury via modulation of CD38-Sirt3 signaling. Methods: Male Sprague Dawley rats were assigned to three groups, (1) Control, (2) Cisplatin (5 mg/kg), and (3) Pretreatment with apigenin (50 mg/kg/day) plus cisplatin groups. Then, left ventricular (LV) function, cardiac injury, oxidative stress, inflammation, apoptosis, and CD38-Sirt3 signaling-related proteins were assessed. Results: Cisplatin impaired LV function and induced cardiac injury, oxidative stress, inflammation, and apoptosis in rats. These changes were accompanied by increased cardiac CD38 and decreased cardiac Sirt3 and SOD2 expression. Apigenin significantly improved LV function (%LVEF and %LVFS), reduced cardiac injury (LDH, CK-MB), attenuated oxidative stress, suppressed inflammatory responses (TNF-α, IL-1β, p-NF-κB, TLR-4), and inhibited apoptosis (Bax/Bcl-2, cleaved caspase-3). Notably, apigenin improved cardiac SOD2 expression and reversed the alteration of CD38-Sirt3 signaling in cisplatin-treated rats. Conclusions: This study provides evidence that cisplatin-induced cardiotoxicity is associated with alterations in CD38-Sirt3 signaling. Apigenin attenuated LV dysfunction and cardiac injury, reduced oxidative stress, inflammation, and apoptosis, potentially through CD38-Sirt3 signaling. These findings highlight the cardioprotective potential of apigenin against cisplatin-induced cardiotoxicity. Full article

Background: Oxidative stress and maladaptive cardiac remodeling are key contributors to heart failure progression. Xestospongia testudinaria, a marine sponge rich in bioactive compounds, possesses antioxidant and lipid-modulating properties. This study investigated the cardioprotective and antioxidant effects of Xestospongia testudinaria methanolic extract (Xesto) in an isoprenaline-induced rat model of heart failure. Methods: Thirty-five healthy male Wistar rats weighing 200–250 g were used in this study. Heart failure was induced in rats via subcutaneous administration of isoprenaline (10 mg/kg/day) for 14 days. Rats were subsequently treated with Xesto (15 mg/kg/day, oral gavage), digoxin (10 mg/kg/day), or saline for an additional 14 days. Hemodynamic parameters, serum NT-proBNP, oxidative stress biomarkers, biochemical indices, hematological parameters, and histopathological changes were evaluated. Molecular docking was performed to assess the interaction of Xesto constituents with Kelch-like ECH-associated protein 1 (KEAP1). Results: Isoprenaline administration significantly increased blood pressure, NT-proBNP, malondialdehyde, hepatic enzymes, and urea levels, while reducing superoxide dismutase and catalase activities. Xesto treatment significantly improved hemodynamic parameters, restored antioxidant enzyme activities, reduced lipid peroxidation, and normalized biochemical and hematological alterations. Histological analysis demonstrated reduced cardiomyocyte hypertrophy and collagen deposition in Xesto-treated rats. Docking analysis showed favorable binding of trans-phytol within the KEAP1 Kelch domain, suggesting possible modulation of antioxidant regulatory pathways. Conclusions: Xestospongia testudinaria exhibited significant cardioprotective and antioxidant effects in isoprenaline-induced heart failure, potentially through enhancement of endogenous antioxidant defenses and attenuation of pathological cardiac remodeling. These findings support its potential as a marine-derived therapeutic candidate for oxidative stress-associated cardiovascular disorders. Full article

Diabetic cardiomyopathy (DCM) under glucolipotoxic stress is sustained by a reactive oxygen species (ROS)-driven circuit in which oxidative DNA damage and nitrosative injury prime NLR family pyrin domain containing 3 (NLRP3) inflammasome assembly, triggering caspase-1 activation, gasdermin D (GSDMD) cleavage, and pyroptotic cardiomyocyte death that propagates apoptosis and fibrotic remodeling. Whether melatonin can disrupt this oxidative-pyroptotic axis when both hyperglycemia and dyslipidemia coexist, the metabolic context most refractory to current therapy has not been established. Apolipoprotein E-deficient (ApoE⁻/⁻) mice were subjected to streptozotocin-induced hyperglycemia and high-fat diet-induced dyslipidemia, then treated with oral melatonin (20 mg/kg/day) for 8 weeks. Despite unchanged fasting glycemia, melatonin attenuated cardiac oxidative stress, reducing 8-OHdG and inducible nitric oxide synthase while restoring Nrf2. Suppression of nuclear factor-κB and NLRP3 was accompanied by lowered interleukin-1β, caspase-1, and GSDMD, indicating disrupted inflammasome priming and pyroptotic execution. Downstream pathology was concurrently attenuated, with reduced TUNEL-positive cardiomyocytes, normalized Bax/Bcl-2 ratio, lower natriuretic peptide expression, diminished interstitial fibrosis, and improved electrocardiographic parameters. These findings position melatonin as a cardioprotective agent that operates despite persistent fasting hyperglycemia, acting through combined attenuation of lipid burden, cumulative glycemic stress, oxidative stress, and inflammatory signaling to arrest downstream apoptotic and fibrotic remodeling under glucolipotoxic conditions, providing a mechanistic rationale for adjunctive melatonin therapy in DCM. Full article

Chagas disease, caused by Trypanosoma cruzi, remains a major public health problem in Latin America and an emerging global health concern due to population mobility. Although benznidazole and nifurtimox remain the only approved antiparasitic drugs, their limited efficacy in chronic infection, prolonged treatment regimens, frequent adverse effects, and variable activity across parasite strains highlight the need for new therapeutic strategies. In addition, the pathogenesis of chronic Chagas disease is driven not only by parasite persistence but also by immune-mediated tissue damage, particularly in chronic Chagas cardiomyopathy. In this review, we examine emerging therapeutic approaches that extend beyond conventional trypanocidal chemotherapy, with emphasis on natural products, antimicrobial peptides, and cell-based immunomodulatory strategies. Plant compounds and essential oils have shown antiparasitic activity through mechanisms including oxidative stress induction, membrane disruption, interference with sterol biosynthesis, and mitochondrial dysfunction, while some extracts also modulate host immune responses. Antimicrobial peptides display dual potential by directly damaging parasite membranes and organelles or by reshaping infection-associated inflammatory responses. In parallel, cell-based therapies such as mesenchymal stromal cells, tolerogenic dendritic cells, and bone marrow-derived cells have demonstrated promising cardioprotective and immunoregulatory effects in experimental chronic Chagas disease. Collectively, these approaches support a multitarget therapeutic framework in which parasite-directed and host-directed interventions may complement each other. Further mechanistic studies, standardization, and translational validation will be essential to advance these candidates toward clinically useful therapies for Chagas disease. Full article

Background: Type 2 diabetes mellitus is associated with chronic low-grade inflammation contributing to endothelial dysfunction, metabolic imbalance, and cardiovascular complications. Although semaglutide (SEM) and tirzepatide (TIR) provide important metabolic and cardioprotective benefits, their early anti-inflammatory effects and potential sex-dependent differences remain incompletely understood. This study comparatively evaluated the effects of SEM and TIR on systemic inflammatory biomarkers in a murine model of streptozotocin-induced diabetes mellitus. Methods: Thirty BALB/c mice were allocated into six experimental groups according to sex and treatment: control, SEM, and TIR groups (n = 5/group). Diabetes was induced by intraperitoneal streptozotocin administration, followed by treatment with SEM or TIR. Circulating interleukin-1β (IL-1β) and pentraxin-3 (PTX-3) levels were measured at baseline, one week after streptozotocin administration, and after six weeks of treatment. Results: Control groups exhibited progressive increases in IL-1β and PTX-3 levels, indicating sustained inflammatory activation. In contrast, SEM- and TIR-treated animals showed attenuated inflammatory responses characterized by transient or stabilized biomarker profiles. Differential inflammatory responses were observed between treatments and sexes. Male SEM and Male TIR groups demonstrated stable IL-1β levels, whereas female treated groups showed persistent elevations, particularly Female TIR animals. PTX-3 responses also displayed differential sex-dependent patterns, with Female SEM animals exhibiting the most stable inflammatory profile. Conclusions: These findings suggest differential early immunomodulatory effects of the two modern antidiabetic drugs, characterized by distinct biomarker responses according to sex and inflammatory marker profile. IL-1β and PTX-3 may represent complementary biomarkers for the assessment of early inflammatory activation associated with diabetes mellitus and its cardiometabolic complications. Full article

The mechanisms underlying doxorubicin (DOX) cardiotoxicity include activation of the renin–angiotensin–aldosterone system (RAAS), oxidative stress, mitochondrial dysfunction, calcium overload, and cardiomyocyte apoptosis. Cortisol plays a key role in regulating multiple metabolic, immunological, cardiovascular, and neuroendocrine processes and may additionally influence drug pharmacokinetics by modulating the activity of P-glycoprotein (P-gp). The peptide apelin, through its specific target, angiotensin II protein J receptor (APJ), exerts cardioprotective, antifibrotic, and anti-inflammatory effects. The available data demonstrate that apelin signaling protects against DOX-induced cardiotoxicity, impacts cortisol secretion, and inhibits RAAS. Short-term elevation in cortisol levels, caused by apelin, may reduce inflammation and thus have cardioprotective properties. However, through chronically elevated cortisol levels, apelin may indirectly contribute to peripheral resistance, cardiac remodeling, and myocardial damage, especially when cortisol metabolism by 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) is altered. This narrative review explores the potential molecular and cellular mechanisms shaping the outcome of apelin–cortisol interplay, offering a potential foundation for developing cardioprotective strategies during anticancer therapy. Future studies should be aimed at assessing the complex interactions between cortisol, apelin, and the RAAS regarding DOX-induced cardiotoxicity. Full article

Background: Designing studies to increase knowledge of the beneficial effects of volatile halogenated anaesthetics(VHAs) is critical to understand the mechanisms activated by myocardial conditioning during ischaemia-reperfusion(I/R) injury. Our research group has identified specific enzymes associated with the SAFE/RISK signalling pathways involved in halogen-induced cardioprotection and has observed a direct correlation between the expression of specific microRNA(miRNAs) and the cardioprotective effect conferred by VHA. Objective: This protocol study has been designed to increase knowledge regarding the cardioprotective effects generated by induced cardioprotective miRNAs after exposure to halogenated drugs without subjecting the patient to additional surgical procedures. Methods: The experimental design that is proposed will be performed with isogenic Wistar rats, all subjected to an I/R procedure. The animals will be randomly divided into two groups: the Donor group and the Recipient group. Half of the rats included in both groups will be exposed to sevoflurane (S), a hypnotic drug, during the I/R procedure, and the other half will be injected with propofol (P), a hypnotic. EVs will be isolated from plasma samples extracted from rats in the Donor group 24 h after the I/R procedure. In vitro EV characterisation will be performed by conducting an ultramorphological analysis, identifying the EV immunophenotype, and quantifying miRNAs. Cardiac function will be assessed by transthoracic echocardiography, histological, and immunohistochemical analyses. Results: The results derived from studies conducted according to this experimental design will support its validation as a preclinical study by regulatory authorities for approval and will serve to design a Phase I clinical trial. Conclusions: The proposed scientific rationale of applying this proposed experimental design will enable the generation of knowledge ‘from the bench to the bedside’ regarding miRNAs with cardioprotective properties induced by exposure to halogenated agents, which could be considered as biomarkers of cardioprotection. Furthermore, biomarker administration could reduce cardiac damage in patients undergoing additional cardiac surgery. Full article

Myocardial ischemia–reperfusion injury (MIRI) represents a major contributor to morbidity and mortality in patients undergoing reperfusion therapy after acute myocardial infarction. Although timely restoration of coronary blood flow is essential for myocardial salvage, reperfusion paradoxically initiates a complex cascade of molecular and cellular events that may aggravate myocardial injury. Oxidative stress is considered one of the central mechanisms underlying MIRI, primarily through excessive production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), leading to mitochondrial dysfunction, calcium overload, endothelial injury, inflammatory activation, and cardiomyocyte death. This review summarizes the current understanding of the pathophysiological mechanisms involved in oxidative stress-mediated reperfusion injury, with emphasis on mitochondrial permeability transition pore opening, inflammasome activation, cytokine release, neutrophil extracellular trap formation, macrophage polarization, and interconnected cell death pathways including PANoptosis. Emerging evidence regarding immunometabolic regulation and epigenetic modulation in MIRI is also discussed. In addition, current pharmacological and non-pharmacological cardioprotective strategies targeting oxidative stress, mitochondrial dysfunction, and inflammatory signaling are reviewed, highlighting both promising experimental findings and the persistent challenges in clinical translation. A deeper understanding of the molecular interplay between oxidative stress and inflammatory pathways may facilitate the development of integrated therapeutic approaches aimed at improving myocardial recovery and long-term cardiovascular outcomes following reperfusion therapy. Full article

Enriching meat with n-3 polyunsaturated fatty acids (n-3 PUFAs) is of considerable nutritional interest because of the well-documented cardioprotective and anti-inflammatory properties of these fatty acids in the human diet. This study investigated the potential effects of dietary Artemisia ordosica Krasch (ARI) supplementation on muscle n-3 PUFA deposition in Albas White Cashmere goats, possibly mediated through the regulation of antioxidant capacity, lipid oxidation, and metabolism. Under the present experimental conditions, ARI supplementation did not significantly affect growth performance, but significantly reduced ruminal C18:0 content (p < 0.05) and increased n-3 PUFA levels (C18:3n3, C22:6n3) in rumen fluid, plasma, liver, and Longissimus dorsi, and the consequent elevation of the muscle PUFA-to-saturated fatty acid ratio (P/S; p < 0.05). Concurrently, ARI supplementation enhanced ruminal and systemic antioxidant capacity, as evidenced by increased glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities, elevated total antioxidant capacity (T-AOC), and upregulated expression of antioxidant-related genes (GSR, GOR, SOD2). Integrated multi-omics analyses revealed that these improvements may be associated with the reduced relative abundance of the core biohydrogenating bacterium s_Butyrivibrio_fibrisolvens and de novo saturated fatty acid synthesis, and potential involvement of the AMPK signaling pathway, with downregulation of FASN; coordinated upregulation of CD36, ACSL3/4, and ELOVL6/7; and upregulation of PPARGC1A, collectively suggesting a promotion of FA oxidation and n-3 PUFA deposition. Collectively, these findings suggest that ARI-promoted n-3 PUFA enrichment in goat meat may be associated with the coordinated modulation of ruminal biohydrogenation, systemic antioxidant capacity, and intermediary lipid metabolism, providing a potential nutritional strategy for developing functional cashmere goat meat. Full article

Obesity increases susceptibility to ventricular arrhythmias due to an arrhythmogenic substrate by promoting oxidative stress and inflammation-driven cardiac remodeling. Klotho, an anti-aging protein that is reduced in obesity-related cardiovascular disease, protects against oxidative injury and inflammation. Berberine (BBR) has been demonstrated to have antiarrhythmic properties, but Klotho mediates these effects in obesity remains unclear. Here, high-fat diet (HFD)-induced obese rats were treated with BBR for 8 weeks. Surface electrocardiography showed BBR shortened prolonged QT, QTc, and Tp-Te intervals. Optical mapping of isolated hearts revealed that BBR eliminated arrhythmia susceptibility (60% to 0%) and stabilized cardiac electrophysiology by shortening action potential duration (APD₅₀/APD₉₀), reducing repolarization dispersion, normalizing conduction velocity, and improving abnormal intracellular Ca²⁺ handling. BBR also attenuated cardiac hypertrophy and fibrosis and increased expression of the potassium channel subunits Kv4.2, Kv4.3, and KChIP2. Furthermore, BBR suppressed oxidative stress and inflammation while upregulating circulating and tissue Klotho levels in obese rats. In ox-LDL-treated H9C2 cells, Klotho silencing abolished the antioxidative and anti-inflammatory effects of BBR, indicating that Klotho is required for its cardioprotective actions. These findings demonstrate that BBR stabilizes the arrhythmogenic substrate in obesity-related cardiac remodeling, at least partly through upregulation of Klotho expression and subsequent attenuation of oxidative stress and inflammation. Full article

Tomatoes (Solanum lycopersicum L.) are one of the most important dietary sources of carotenoids, especially lycopene, a bioactive compound associated with antioxidant, anti-inflammatory and cardioprotective effects. This review synthesizes recent data on the phytochemical composition of tomatoes, with a focus on lycopene, its main biological mechanisms and health benefits, including the reduction in oxidative stress. The manuscript also highlights the influence of thermal processing and food matrix on the bioavailability of lycopene, as well as the role of innovative formulation and nanoencapsulation systems in increasing its stability and absorption. Modern extraction and analysis methods are also presented, including ultrasound, microwave and supercritical-fluid-assisted techniques, along with HPLC chromatographic methods. A distinctive element is the analysis of lycopene-based food supplements available on the markets in Romania, Europe and the United States, from the perspective of composition, standardization and safety. Current data support the potential of lycopene as a valuable nutraceutical ingredient, but further clinical studies are needed to confirm therapeutic benefits. Full article