TL;DR
In general, epigenetic regulation provides a new conceptual framework for understanding TEC dysfunction in DKD and provides a potential direction for the development of precision therapeutic strategies.
A narrative review elaborates the closed-loop crosstalk between mitochondrial metabolism and epigenetics in tubular injury, highlights the therapeutic prospect of targeting this bidirectional regulatory axis, and provides novel theoretical evidence for revealing DKD pathogenesis and developing targeted intervention regimens.
This review systematically examines the mechanisms of metabolic reprogramming in different renal cell types and highlights their contribution to renal injury, highlighting the ability of natural products to confer renal protection by modulating key regulatory nodes of metabolic reprogramming.
Multi-omics integration and spatial transcriptomics hold promise for individualized and mechanism-guided interventions to halt diabetic kidney disease progression and propose precision strategies targeting mitochondrial homeostasis, ferroptosis inhibition, glycolytic blockade in immune cells, and multimodal therapies.
This review integrates current insights into the complex interplay among metabolic stress, mitochondrial injury, and cellular senescence in Diabetic cardiomyopathy and highlights promising directions for mechanism-based interventions aimed at combating diabetic cardiac remodeling.
The cellular and molecular mechanisms of EndMT relevant to CKD are summarized, key regulatory pathways and pathway crosstalk are highlighted, and emerging pharmacological approaches to limit EndMT, preserve microvascular integrity, and attenuate renal fibrogenesis are discussed.
Liver fibrosis is a common consequence of chronic liver injury and a major contributor to liver‐related mortality. Persistent hepatocellular injury promotes fibrosis initiation and progression through excessive extracellular matrix deposition. Hepatic stellate cells (HSCs), the principal source of extracellular matrix in the fibrotic liver, transition from a quiescent state to an activated myofibroblast‐like phenotype in response to profibrotic stimuli such as transforming growth factor‐beta. This transition is accompanied by transcriptional and epigenetic reprogramming involving DNA methylation, histone modifications, and regulation by non‐coding RNAs. Treating the underlying cause of liver disease, such as promoting weight loss in metabolic dysfunction‐associated steatohepatitis or eradicating viral hepatitis, remains the principal strategy for slowing or potentially reversing fibrosis. Despite substantial advances in understanding the cellular and molecular basis of liver fibrosis and HSC activation, most mechanism‐based therapeutic approaches have not yet demonstrated clinical efficacy. Further translational and clinical studies are therefore required. Recent advances in molecular biology have highlighted the potential relevance of epigenetic modifications to the diagnosis, treatment, and prognosis of chronic liver disease. In this review, we summarize the principal epigenetic changes involved in HSC activation, and initiation/progression of liver fibrosis. We also discuss recent interventions designed to modulate these epigenetic changes and evaluate their therapeutic potential in experimental models of liver fibrosis.
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