Integrative Insights Into Mitochondrial Dysfunction and Organelle Crosstalk in Diabetic Kidney Disease - PubMed
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- #mitochondrial dysfunction
- #diabetic kidney disease
- #organelle crosstalk
- Diabetic kidney disease (DKD) is a leading cause of end-stage kidney disease, driven by mitochondrial dysfunction.
- Mitochondrial dysfunction in DKD leads to metabolic reprogramming, oxidative stress, and inflammation, accelerating kidney injury.
- Key mitochondrial mechanisms in DKD include metabolic reprogramming, altered fission-fusion dynamics, defective mitophagy, and mtDNA release.
- Mitochondria-ER contacts (MAMs) integrate redox signaling and calcium homeostasis, playing a critical role in DKD progression.
- Preclinical interventions targeting mitochondrial biogenesis, dynamics, mitophagy, and mtDNA preservation show promise in attenuating kidney injury.
- Clinically, drugs like metformin, SGLT2 inhibitors, finerenone, and GLP-1RAs exert renoprotective effects via mitochondrial pathways.
- Emerging therapies include targeted antioxidants, metabolic activators, fission inhibitors, and mitochondrial transplantation.
- A translational framework links mitochondrial mechanisms to therapeutic strategies for DKD.