Table 4.

Non-coding RNAs linked to renal mito epigenetic regulation.

RNA	Disease/model	Target cell/context	Mitochondria-associated action	Epigenetic/regulatory role	Downstream phenotype	Evidence type
miR-21	DKD, CKD, Alport/fibrosis models	Tubules, fibroblasts, glomerular compartments	Suppresses metabolic pathways; associated with mitochondrial dysfunction	Post-transcriptional control of profibrotic signaling	TGF-β amplification, fibrosis, ECM deposition	Intervention-supported in animal models (51, 76, 95)
miR-192	Diabetic nephropathy	Mesangial and tubular contexts	Indirect metabolic stress association	TGF-β-responsive miRNA network	Matrix expansion and fibrosis	Experimental and associative (25, 88)
miR-34a	DKD/renal apoptosis contexts	Tubular cells and podocyte stress	Apoptosis and mitochondrial injury association	p53-linked regulatory circuit	Cell death and impaired repair	Experimental; renal specificity and direction vary by model (96)
miR-155	Inflammatory kidney injury	Immune and renal inflammatory compartments	Immunometabolic activation	Inflammatory transcript regulation	Cytokine production and macrophage activation	Experimental/associative (51)
TUG1	Diabetic nephropathy	Podocyte/tubular metabolic stress	Regulates mitochondrial bioenergetics	lncRNA control of transcriptional/metabolic networks	Bioenergetic preservation or dysfunction depending on expression	Mechanistic animal/cell evidence (97)
MALAT1/NEAT1	Inflammation and fibrosis models	Tubules and immune-interacting compartments	Oxidative stress and inflammasome association	lncRNA scaffolding/regulatory effects	Inflammation, fibrosis, cellular stress	Experimental; disease specificity incomplete (52)
circRNAs	Emerging renal disease studies	Cell-type dependent	Potential miRNA sponge effects on mitochondrial and fibrotic targets	Post-transcriptional regulatory hubs	Fibrosis/inflammation hypotheses	Emerging; direct renal functional validation limited