Table 1.

Organelle stress and its phenotypic changes in kidney diseases.

Kidney Disease Pathogenic Phenotypes	Organelle Dysfunction	Organelle Phenotypic Changes	Ref.
Acute Kidney Injury (AKI)
Ischemia-reperfusion	Mitochondria	↑Mitochondrial fission (Fragmentation) ↓ATP production	[17,18] [17,18]
Cisplatin	Mitochondria	↑Mitochondrial DNA-ER-mediated inflammation	[19]
Chronic Kidney Disease (CKD)
Diabetic glomerular cell damage	Mitochondria	↑Mitochondrial fission (Fragmentation)	[20]
Diabetic tubular cell damage	Mitochondria ER ER-Mitochondria	Aberrant TCA cycle ↑Mitochondrial fission (Fragmentation) ↑Mitochondrial ROS ↓ATP production ↓Lipid β-oxidation ↑Unfolded protein response (UPR) ↓Organelle contact sites (MAM)	[21,22] [23,24] [23,24] [23,24] [14,25] [25] [25]
AKI (ischemia-reperfusion)-to-CKD transition	Mitochondria ER- Mitochondria	↑Mitochondrial fission (Fragmentation) ↓Lipid β-oxidation (lipotoxicity)	[26] [27]
Autosomal dominant polycystic kidney disease (ADPKD)	Primary cilia-mitochondria	↓Glucose metabolism ↓Lipid β-oxidation ↑Mitochondrial ROS ↑Mitochondrial fission (Fragmentation) Impaired Ca homeostasis	[28] [29,30,31,32] [33,34] [33,34] [35,36]

ER; endoplasmic reticulum, ROS; reactive oxygen species, MAM; mitochondria-associated ER membranes.