Hodgkin lymphoma (HL) is a highly curable malignancy and increasing survival rates have shifted attention towards long-term treatment-related complications, particularly infertility among young women of reproductive age. Chemotherapy-induced ovarian damage is a multifactorial process that may lead to diminished ovarian reserve, premature ovarian failure, and impaired fertility. Several distinct mechanisms contribute to ovarian injury. Direct DNA damage to primordial follicles is the best-characterized pathway, resulting in apoptosis and irreversible depletion of the follicular pool. Chemotherapy also affects granulosa cells and ovarian stromal tissue, disrupting the microenvironment necessary for follicular growth and hormone production. In addition, vascular injury characterized by endothelial dysfunction, reduced ovarian perfusion, and cortical fibrosis may compromise follicular survival and contribute to long-term ovarian dysfunction. More recently, dysregulation of the PI3K/PTEN/Akt/mTOR signaling pathway has emerged as an important mechanism, promoting accelerated activation and premature exhaustion of primordial follicles, a phenomenon known as the "burnout effect." These mechanisms frequently coexist and their relative contribution depends on treatment intensity, cumulative drug exposure, and patient-specific factors. Current fertility preservation strategies include oocyte, embryo, and ovarian tissue cryopreservation, while the uncertain efficacy of pharmacological ovarian suppression in HL highlights the need for further research into effective gonadoprotective approaches. This review summarizes current evidence regarding the biological mechanisms underlying chemotherapy-induced ovarian damage in women with HL and discusses their implications for fertility preservation and long-term reproductive health.

There is an extensive pipeline of therapies for diabetes mellitus. It has been known for the past three decades that obesity is a key pathophysiological player, involving inflammation, insulin resistance and metabolic dysfunction leading to type 2 diabetes and to significant cardiovascular, renal and hepatic complications, all central to the metabolic syndrome. On the basis of this knowledge and the disposition of drugs with multiple effects on different disease components, the diabetes therapeutic paradigm has shifted from merely glucocentric to multitargeted against these interconnected pathways.Much more recently, incretin-based multi-agonists have been developed that deliver unprecedented glycemic and weight benefits as well as weekly insulins and oral GLP-1 agonists that are able to reduce the burden of injectable therapies. An antibody-peptide conjugate that acts as a dual GLP-1/GIP receptor modulator has also shown promising results. Today, novel insulin sensitizers are modulating metabolic pathways towards higher energy expenditure with fewer side effects. Adjunctive agents for type 1 diabetes are improving glucose control while reducing hypoglycemia risk. Finally, drugs designed to restrain the inevitable muscle mass loss caused by antiobesity treatments are being tested. The diabetes pipeline is rich and there is hope that in the next few years, the therapeutic landscape will be further transformed with even more efficacious and individualized treatments.

Type 2 diabetes mellitus (T2DM) develops through the interplay of insulin resistance and progressive beta-cell dysfunction. Beyond genetic predisposition, epigenetic regulation provides a mechanistic link between environmental exposures (e.g., overnutrition, physical inactivity, inflammation) and durable changes in gene expression in pancreatic islets and insulin-sensitive tissues (skeletal muscle, adipose tissue, and liver). Accordingly, this review aims to synthesize current evidence on the epigenetic mechanisms underlying T2DM and its complications, with a particular focus on epigenetically targeted therapeutic strategies. We summarize major epigenetic processes, including DNA and RNA methylation, histone post-translational modifications, and non-coding RNAs, and discuss how these alterations remodel chromatin and transcriptional programs under metabolic stress. A key concept is "metabolic memory," whereby transient hyperglycemia or lipotoxicity can induce persistent epigenetic signatures that sustain dysfunctional cellular phenotypes, partly shaped by mitochondrial metabolism and Krebs cycle intermediates regulating chromatin-modifying enzymes. Importantly, several epigenetic alterations demonstrate partial reversibility following lifestyle modification, metabolic surgery, or pharmacological intervention (e.g., DNA methyltransferase inhibition), underscoring their therapeutic relevance. Finally, we address translational challenges, including limited access to human tissues and inadequate modeling of chronic metabolic stress, which currently constrain clinical exploitation of epigenetic targets in T2DM.

Type 2 diabetes (T2D) is a chronic metabolic disorder primarily affecting the metabolism of glucose in the body. It is characterized by polyphagia, polydipsia, polyuria, fatigue, and persistent hyperglycemia. It occurs mainly because of two major factors, namely, dysregulated insulin secretion from pancreatic β-cells and/or reduced sensitivity of insulin-responsive tissues to insulin, i.e., insulin resistance. The process of insulin secretion and insulin signaling is complex, requiring the involvement of distinct membrane receptors. Sulfonylureas are a class of antidiabetic drugs which exert their antidiabetic action by stimulating sulfonylurea receptors on the pancreatic β-cells. Other cellular mechanisms mediated by receptors, such as insulin receptor, glucagon-like peptide-1 receptor, free fatty acid receptors, and peroxisome proliferator-activated receptor-γ, also serve as potential therapeutic targets for a number of conventional and novel antidiabetic agents. In this review article, we discuss the significance of these receptors in the therapeutic regulation of T2D. We also lay emphasis on the need for the development of novel antidiabetic agents, several of which are currently advancing through clinical research to determine their potential for antidiabetic mediation through these receptors.