Mitochondrial dysfunction and abnormal lipid accumulation may accelerate early .
Evidence
This review summarizes current literature on diabetic kidney disease, renal tubular mitochondrial bioenergetics, mtROS, autophagy, and lipid metabolism disorders.
Caveat
The abstract states that the mechanisms of renal tubular mitochondrial dysfunction and lipid-metabolism regulation remain incompletely elucidated.
Simplified
Diabetic kidney disease (DKD) is a common and serious microvascular complication in patients with diabetes. In recent years, has emerged as a major research focus, as its prognosis is closely associated with tubular atrophy and interstitial fibrosis. Multiple studies indicate that diabetes directly damages renal tubules, leading to mitochondrial dysfunction-characterized by impaired mitochondrial bioenergetics, excessive mitochondrial (mtROS) production, defective autophagy, and lipid metabolism disorders resulting from abnormal lipid accumulation. Consequently, this cascade triggers a series of metabolic abnormalities. However, the precise mechanisms underlying renal tubular mitochondrial dysfunction and the regulatory pathways of lipid metabolism disorders remain incompletely elucidated. A deeper understanding of the pathobiology of the tubulointerstitium will facilitate the discovery of novel biomarkers for DKD. Based on current literature, this review proposes that mitochondrial dysfunction and abnormal lipid metabolism may accelerate early-stage diabetic tubulopathy, thereby potentially improving patient prognosis.
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