Recent advances in epigenetics indicate that several epigenetic modifications, including acetylation, methylatio, and microRNA (miRNA), play an important role in the pathogenesis of acute kidney injury (AKI). Our study reveales that enhancement of protein acetylation by pharmacological inhibition of class I histone deacetylases leads to more severe tubular injury, and delays the restoration of renal structure and function. The changes in promoter DNA methylation occurs in the kidney with ischemia/reperfusion. MiRNA expression is associated with the regulation of both renal injury and regeneration after AKI. Targeting the epigenetic process may provide a therapeutic treatment for patients with AKI. The purpose of this review is to summarize recent advances in epigenetic regulation of AKI and provide mechanistic insight into the role of acetylation, methylation, and miRNA expression in the pathological processes of AKI.
Retinoblastoma (RB) is a common intraocular tumor in children, often leading to blindness or disability, and its pathogenesis involves genetic and epigenetic regulation. Epigenetics regulates gene expression through mechanisms such as DNA methylation and histone modification without altering the DNA sequence, and the imbalance of its homeostasis is considered a crucial factor in the development and progression of RB. Therapeutic strategies targeting these abnormal modifications offer new potential treatment avenues for RB. Although current research has highlighted the importance of epigenetics in RB, the specific mechanisms of action, the relationship with genetic bases, and the development of targeted drugs remain largely unknown. Therefore, further in-depth research into the epigenetic mechanisms of RB is of great significance for elucidating its carcinogenic mechanisms, identifying effective therapeutic targets, and developing new drugs.
Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes, characterized by high blindness rates and a severe impact on patients' quality of life. Despite adequate glycemic control, some patients exhibit persistent progression of retinal microvascular damage, known as the "metabolic memory" phenomenon. Studies have revealed that the essence of this phenomenon is the sustained expression of epigenetic reprogramming induced by metabolic stress, in which abnormal mitochondrial DNA (mtDNA) methylation plays a pivotal role. Metabolic abnormalities such as hyperglycemia, hyperhomocysteinemia, and hyperlipidemia can alter mtDNA methylation patterns, triggering cascading pathological processes including oxidative stress, chronic inflammation, and neurovascular network disorders, remodeling mitochondrial energy metabolism, and promoting the evolution of DR from subclinical compensatory stage to irreversible structural damage. Abnormal mtDNA methylation serves as a hallmark of metabolic memory and a core driver of microvascular lesions, providing an important theoretical basis for in-depth analysis of metabolic memory mechanisms and exploration of DR intervention strategies. Current research needs to further elucidate its role in DR. Future efforts require integration of multi-dimensional epigenetic biomarkers, precise intervention approaches, and clinical translational research to advance the early diagnosis and individualized treatment of DR.