Cardiovascular illnesses remain the primary cause of death, accounting for at least 17.9 million fatalities per year and posing a significant public health problem because of its extensive predominance and effect on healthcare systems. The etiology of cardiovascular disease is complex and involves several environmental and lifestyle factors. Alcohol use is a highly important determinant because of its dual-edged effect on cardiovascular health. Multiple studies indicate that moderate alcohol consumption may have certain advantages, such as slight enhancements in lipid profiles. Conversely, excessive alcohol intake is associated with serious negative consequences, including cardiomyopathy, hypertension, arrhythmias, and even mortality. The aim of this study is to provide a comprehensive analysis of the several effects of alcohol on cardiovascular health and their understanding within the medical field over time. It uses an interpretative narrative review methodology and analyzes studies that focus on genetic risk factors, gender differences, and shifts in paradigms in recent years. This article highlights the need for obtaining a thorough understanding of the effects of alcohol on cardiovascular health to support public health guidelines and clinical practice, and it underscores the significance of including alcohol consumption into the broader context of cardiovascular risk management and identifies important subjects for further study.

Ischemic stroke (IS) remains a leading cause of long-term disability and mortality worldwide, with recovery outcomes shaped by the interplay between acute vascular injury, pre-existing comorbidities, and individual molecular profiles. Common risk factors-such as diabetes mellitus, atrial fibrillation, hypertension, and dyslipidemia-not only increase stroke susceptibility but also impair neurovascular repair by perpetuating systemic inflammation, endothelial dysfunction, and impaired neuroplasticity. Aging remains an underexplored determinant of epigenetic remodeling in stroke. Beyond these clinical determinants, genetic and epigenetic mechanisms contribute substantially to stroke heterogeneity. Genome-wide association studies (GWAS) have identified loci such as HDAC9, PATJ, PTCH1, and ABO that modulate inflammation, oxidative stress, and vascular remodeling. Complementary epigenetic pathways, including DNA methylation, histone acetylation, and circular RNAs (circRNAs), dynamically regulate gene expression in response to ischemia and comorbid influences, encoding a persistent "molecular memory" that shapes both injury and repair. Functional studies reveal that circRNAs orchestrate apoptosis, angiogenesis, and synaptic remodeling, while selective DNMT and HDAC inhibition can restore neurovascular integrity in experimental models. Recent multi-omics and longitudinal approaches demonstrate that these molecular signatures evolve across acute, subacute, and chronic phases of recovery, yet clinical translation remains limited. Aging and chronic comorbidities further modify epigenetic programs, reducing repair capacity. Although genotype-guided antiplatelet therapy illustrates the feasibility of personalized stroke care, broader genomics- and epigenetics-informed interventions require rigorous validation. This review integrates current knowledge on the interplay between vascular comorbidities, genetic predisposition, and epigenetic regulation in shaping stroke recovery. Understanding these interactions is essential for developing precision medicine approaches that enhance functional outcomes and reduce recurrence in stroke survivors.Integrating multi-omics profiling with comorbidity stratification, functional validation, and longitudinal biomarker tracking will be pivotal to achieving actionable precision medicine and improving outcomes in stroke survivors.

Carpal Tunnel Syndrome (CTS) is a prevalent neuropathic disorder caused by chronic compression of the median nerve, leading to sensory and motor impairments. Conventional treatments, such as corticosteroid injections, wrist splinting, and surgical decompression, often fail to provide adequate outcomes for chronic or recurrent cases, emphasizing the need for innovative therapies. Hydrogels, highly biocompatible three-dimensional biomaterials with customizable properties, hold significant potential for CTS management. Their ability to mimic the extracellular matrix facilitates localized drug delivery, anti-adhesion barrier formation, and tissue regeneration. Advances in hydrogel engineering have introduced stimuli-responsive systems tailored to the biomechanical environment of the carpal tunnel, enabling sustained therapeutic release and improved tissue integration. Despite these promising developments, hydrogel applications for CTS remain underexplored. Key challenges include the absence of CTS-specific preclinical models and the need for rigorous clinical validation. Addressing these gaps could unlock the full potential of hydrogel-based interventions, which offer minimally invasive, customizable solutions that could improve long-term outcomes and reduce recurrence rates. This review highlights hydrogels as a transformative approach to CTS therapy, advocating for continued research to address translational barriers. These innovations have the potential to redefine the treatment landscape, significantly enhancing patient care and quality of life.

Chronic wounds, diabetic foot ulcers, venous leg ulcers, and pressure injuries affect millions of patients worldwide and cost healthcare systems in the order of $150 billion annually, yet treatment options have changed less than the scale of the problem would suggest. Biofilm formation, documented in up to 78% of chronic wounds, is a central cause: bacteria embedded in extracellular polymeric matrices tolerate antimicrobial concentrations up to 1000-fold higher than planktonic cells and sustain a chronic inflammatory state that actively prevents tissue repair. Hydrogels, crosslinked polymer networks with high water content and tunable physicochemical properties, have been widely studied as platforms for addressing these challenges, though the distance between laboratory results and clinical practice remains considerable. While recent reviews have summarized hydrogel materials or antimicrobial strategies in isolation, this review takes a different approach: we treat infection, biofilm persistence, and impaired regeneration as interconnected processes that must be addressed simultaneously, and we examine biofilm management as a distinct therapeutic target rather than merely a subset of antimicrobial delivery. We analyze hydrogel-based wound care across three integrated domains: design principles (natural, synthetic, and hybrid polymer systems; crosslinking strategies; and stimuli-responsive architectures), antimicrobial delivery (silver, antibiotics, antimicrobial peptides, natural agents, and controlled-release systems), and biofilm management (nanoparticle-mediated disruption, enzymatic EPS degradation, photodynamic approaches, quorum-sensing inhibition, and anti-adhesive surface engineering). For each area, we critically evaluate what the preclinical evidence supports, where it falls short, and what would be needed to bridge the gap to clinical application. Translation remains uneven. Among the many FDA- and EMA-cleared hydrogel dressings currently in clinical use, most are simple moisture-retaining or silver-containing formulations, while the multifunctional systems that dominate the research literature are at earlier stages of development. We discuss the main translational priorities, including more predictive preclinical models, long-term nanomaterial safety, harmonized outcome reporting, manufacturing scalability, and health economic evidence, as areas where further work can meaningfully accelerate clinical adoption.

Ischemic stroke (IS) remains a leading cause of disability and mortality in aging populations. Recovery trajectories are shaped not only by the acute vascular insult but also by pre-existing comorbidities, genetic predisposition, and age-dependent molecular remodeling. Common vascular risk factors, such as diabetes mellitus, atrial fibrillation, hypertension, and dyslipidemia, sustain systemic and cerebral inflammation, promote endothelial dysfunction, disrupt blood-brain barrier integrity, and impair neuroplasticity, collectively limiting neurovascular repair and recovery potential. Recent advances in genomic, epigenomic, and transcriptomic profiling have identified dynamic molecular networks that regulate neuronal survival, angiogenesis, and synaptic plasticity after stroke. However, most discoveries remain correlative. Establishing causality will require perturbation-based approaches, including genome and epigenome editing, patient-derived stem cell and organoid models, and longitudinal multi-omics analyses across diverse ancestries and comorbidity profiles. Such integration will clarify how metabolic and inflammatory states imprint the epigenetic and transcriptional landscape of the aging brain. Emerging evidence implicates DNA methylation, histone modifications, and noncoding RNAs, including circular RNAs, as pivotal regulators of ischemic resilience and neurovascular recovery. Translational studies combining genomic insights with epigenetic pharmacology have demonstrated proof-of-concept efficacy for genotype-guided therapies, RNA-based interventions, and histone deacetylase inhibition. Collectively, these strategies support a systems-level framework that unites vascular biology, multi-omics, and neurorestoration. Within this paradigm, aging is reframed not as a static risk factor but as a modifiable molecular trait, guiding the timing and intensity of interventions to enhance neurorepair, restore vascular integrity, and preserve cognitive resilience.

Background: During the pandemic, our hospital became a COVID support hospital and consequently the cardiology clinic had restricted activity; thus, it received only suspect and/or patients confirmed positive with the various COVID-19 strains that were associated with a chronic/flaring cardiovascular pathology. Methods: Two batches of patients admitted during a one-year period were compared in the cardiology clinic over two different periods of time: BATCH I (1 April 2019 to 31 March 2020), in a non-COVID context (BATCH I N-COV) and BATCH II (1 July 2020 to 30 June 2021) comprising patients that presented with respiratory infection of SARS-CoV-2 (BATCH II COV-2), associated with chronic and/or acute cardiovascular condition. To determine the profile of the patients admitted in our clinic, we observed the following parameters: age, type of cardiac condition, and admission mode (for the N-COV group). Results: The data obtained as absolute numbers and as percentages in relation to the total number of admissions were presented in separate tables and graphs for both of the studied groups. Conclusions: The SARS-CoV-2 pandemic, in its almost two years of evolution, has divided the medical world in two main categories: COVID and non-COVID. Admission of the patients with chronic, but non-COVID cardiac conditions, in our case, dropped to almost one-quarter when we compared the two absolute admission numbers: 1382 in the year prior to pandemic compared with only 356 in the pandemic year. We believe that the number of deaths due to SARS-CoV-2 infection was infinitely higher than the reported ones and uncountable, in as much as COVID-19 did not kill only the infected patients, but it has also yielded a very large number of collateral victims among chronic patients who had no contact with the disease, but were unable to be admitted and treated for chronic heart disease.