The skin, the largest organ of the human body, plays numerous essential roles, including protection against environmental hazards and the regulation of body temperature. The processes of skin homeostasis and ageing are complex and influenced by many factors, with epigenetic mechanisms being particularly significant. Epigenetics refers to the regulation of gene expression without altering the underlying DNA sequence. The dynamic nature of the skin, characterized by constant cellular turnover and responsiveness to environmental stimuli, requires precise gene activity control. This control is largely mediated by epigenetic modifications such as DNA methylation, histone modification, and regulation by non-coding RNAs. The present review endeavours to provide a comprehensive exploration and elucidation of the role of epigenetic mechanisms in regulating skin homeostasis and ageing. By integrating our current knowledge of epigenetic modifications with the latest advancements in dermatological research, we can gain a deeper comprehension of the complex regulatory networks that govern skin biology. Understanding these mechanisms also presents promising avenues for therapeutic interventions aimed at improving skin health and mitigating age-related skin conditions.

Infertility is a global phenomenon that impacts people of both the male and the female sex; it is related to multiple factors affecting an individual’s overall systemic health. Recently, investigators have been using mesenchymal stem cell (MSC) therapy for female-fertility-related disorders such as polycystic ovarian syndrome (PCOS), premature ovarian failure (POF), endometriosis, preeclampsia, and Asherman syndrome (AS). Studies have shown promising results, indicating that MSCs can enhance ovarian function and restore fertility for affected individuals. Due to their regenerative effects and their participation in several paracrine pathways, MSCs can improve the fertility outcome. However, their beneficial effects are dependent on the methodologies and materials used from isolation to reimplantation. In this review, we provide an overview of the protocols and methods used in applications of MSCs. Moreover, we summarize the findings of published preclinical studies on infertility treatments and discuss the multiple properties of these studies, depending on the isolation source of the MSCs used.

Mitochondrial dysfunction is a key driver of neurological disorders due to the brain’s high energy demands and reliance on mitochondrial homeostasis. Despite advances in genetic characterization, the heterogeneity of mitochondrial diseases complicates diagnosis and treatment. Mitochondrial dysfunction spans a broad clinical spectrum, from early-onset encephalopathies to adult neurodegeneration, with phenotypic and genetic variability necessitating integrated models of mitochondrial neuropathology. Mutations in nuclear or mitochondrial DNA disrupt energy production, induce oxidative stress, impair mitophagy and biogenesis, and lead to neuronal degeneration and apoptosis. This narrative review provides a structured synthesis of current knowledge by classifying mitochondrial-related neurological disorders according to disrupted biochemical pathways, in order to clarify links between genetic mutations, metabolic impairments, and clinical phenotypes. More specifically, a pathway-oriented framework was adopted that organizes disorders based on the primary mitochondrial processes affected: oxidative phosphorylation (OXPHOS), pyruvate metabolism, fatty acid β-oxidation, amino acid metabolism, phospholipid remodeling, multi-system interactions, and neurodegeneration with brain iron accumulation. Genetic, clinical and molecular data were analyzed to elucidate shared and distinct pathophysiological features. A comprehensive table synthesizes genetic causes, inheritance patterns, and neurological manifestations across disorders. This approach offers a conceptual framework that connects molecular findings to clinical practice, supporting more precise diagnostic strategies and the development of targeted therapies. Advances in whole-exome sequencing, pharmacogenomic profiling, mitochondrial gene editing, metabolic reprogramming, and replacement therapy—promise individualized therapeutic approaches, although hurdles including heteroplasmy, tissue specificity, and delivery challenges must be overcome. Ongoing molecular research is essential for translating these advances into improved patient care and quality of life.

Lysosomal storage disorders (LSDs) represent a diverse group of inherited metabolic diseases in which impaired lysosomal function leads to progressive accumulation of undegraded substrates and widespread cellular dysfunction. Although traditionally classified according to the type of stored macromolecule, this substrate-based approach often fails to reflect the underlying molecular mechanisms. Recent advances in genetics and cell biology have prompted a shift toward functional classifications that group disorders by the lysosomal pathway disrupted—namely, enzymatic hydrolytic defects, transporter-related defects, biogenesis and signaling defects, and cross-organelle interaction abnormalities. This framework better captures disease complexity and provides a translational roadmap for precision medicine. The neurological system, with its high metabolic demands and vulnerability to impaired clearance mechanisms, is particularly affected, leading to clinical phenotypes ranging from developmental delay to severe neurodegeneration. Genomic technologies and multi-omics platforms have facilitated earlier diagnoses, revealed atypical variants, and informed the development of tailored therapies such as enzyme replacement, substrate reduction, chaperone-based approaches, and gene therapy. The current review proposes a cellular-pathway-oriented framework for classifying LSDs with neurological features and underscores how such an approach can assist in the development of personalized therapeutic strategies.

Zinc may mitigate platinum-induced toxicity through antioxidant, anti-inflammatory and anti-apoptotic effects. We systematically reviewed preclinical in vivo evidence on zinc-based interventions, focusing on organ protection, mechanisms and antitumour efficacy. PubMed, Scopus, Web of Science and supplementary sources were searched for studies in rats and mice. Risk of bias was assessed using SYRCLE, and the findings were synthesised narratively. Database searches identified 1552 records; 25 studies were included following database and supplementary screening. The risk of bias was frequently unclear for sequence generation, allocation concealment and blinding. Most studies investigated cisplatin; fewer evaluated carboplatin, oxaliplatin or combination chemotherapy. Zinc interventions included salts, dietary supplementation, organic complexes and nanoformulations, predominantly administered before platinum exposure. Protective findings were reported across renal, reproductive, nervous, hepatic, haematopoietic and cardiovascular systems. Proposed mechanisms included metallothionein induction, enhanced antioxidant defences and modulation of inflammation and apoptosis. Heterogeneity precluded conclusions about formulation superiority. Limited tumour-bearing evidence indicated that zinc-induced metallothionein may reduce cisplatin activity, whereas bismuth zinc citrate preserved tumour control within the tested model. Methodological weaknesses, heterogeneity and scarce tumour-bearing evidence limit confidence in efficacy and oncological safety. These findings support further preclinical investigation rather than clinical implementation.