Abstract
Macroautophagy/autophagy is a conserved cellular process that degrades misfolded proteins and damaged organelles to regulate cell survival and division. Normal levels of autophagy are observed in healthy kidney cells. In contrast, excessive or insufficient autophagy is observed during kidney disease progression. However, canonical treatments that regulate autophagy using chemical reagents may induce unexpected side effects in other organs. This necessitates the development of therapeutic approaches with fewer adverse effects. Non-coding RNAs, which are highly tissue-specific, regulate autophagy and accurately modulate the expression of related genes. This review presents evidence of the effects of non-coding RNAs on the progression of kidney diseases and their responses to treatment in vitro, in vivo, and in clinical trials. Our analyses and interpretations of key findings elucidate the pathogenesis of kidney diseases and explore potential new therapeutic approaches.Abbreviations: 3' UTR: 3' untranslated region; 3-MA: 3-methyladenine; ADPKD: autosomal dominant polycystic kidney disease; AKI: acute kidney injury; ccRCC: clear cell RCC; ATG: autophagy related gene; ceRNA: competing endogenous RNA; circRNA: circular RNA; CKD: chronic kidney disease; DKD: diabetic kidney disease; HG: high glucose; IRI: ischemia-reperfusion injury; lncRNA: long non-coding RNA; LPS: lipopolysaccharide; miRNA: microRNA; MTOR: mechanistic target of rapamycin kinase; ncRNA: non-coding RNA; PI3K: phosphoinositide 3-kinase; RCC: renal cell carcinoma; ROS: reactive oxygen species; RTEC: renal tubular epithelial cells; ULK1: unc-51 like autophagy activating kinase 1; UUO: unilateral ureteral obstruction; VHL: von Hippel-Lindau tumor suppressor.