Mitochondrial dysfunction and the AKI-to-CKD transition DOI
Mingzhu Jiang, Mi Bai, Juan Lei

и другие.

AJP Renal Physiology, Год журнала: 2020, Номер 319(6), С. F1105 - F1116

Опубликована: Окт. 19, 2020

Acute kidney injury (AKI) has been widely recognized as an important risk factor for the occurrence and development of chronic disease (CKD). Even milder AKI adverse consequences could progress to renal fibrosis, which is ultimate common pathway various terminal diseases. Thus, it urgent develop a strategy hinder transition from CKD. Some mechanisms AKI-to-CKD have revealed, such nephron loss, cell cycle arrest, persistent inflammation, endothelial with vascular rarefaction, epigenetic changes. Previous studies elucidated pivotal role mitochondria in acute injuries demonstrated that fitness this organelle major determinant both pathogenesis recovery organ function. Recent research suggested damage mitochondrial function early crucial leading tubular insufficiency. Dysregulation homeostasis, alterations bioenergetics, stress cross talk contribute transition. In review, we focus on pathophysiology after progression CKD, confirming targeting represents potentially effective therapeutic

Язык: Английский

Identifying drug targets in tissues and whole blood with thermal-shift profiling DOI

Jessica Perrin,

Thilo Werner, Nils Kurzawa

и другие.

Nature Biotechnology, Год журнала: 2020, Номер 38(3), С. 303 - 308

Опубликована: Янв. 20, 2020

Язык: Английский

Процитировано

159

Cytochrome c phosphorylation: Control of mitochondrial electron transport chain flux and apoptosis DOI Creative Commons
Hasini A. Kalpage, Junmei Wan, Paul T. Morse

и другие.

The International Journal of Biochemistry & Cell Biology, Год журнала: 2020, Номер 121, С. 105704 - 105704

Опубликована: Фев. 2, 2020

Язык: Английский

Процитировано

159

Berberine Protects Glomerular Podocytes via Inhibiting Drp1-Mediated Mitochondrial Fission and Dysfunction DOI Creative Commons
Xin Qin, Yan Zhao, Jing Gong

и другие.

Theranostics, Год журнала: 2019, Номер 9(6), С. 1698 - 1713

Опубликована: Янв. 1, 2019

Elevated levels of plasma free fatty acid (FFA) and disturbed mitochondrial dynamics play crucial roles in the pathogenesis diabetic kidney disease (DKD).However, mechanisms by which FFA leads to damage glomerular podocytes DKD effects Berberine (BBR) on are not fully understood.Methods: Using db/db mice model cultured mouse podocytes, we investigated molecular mechanism FFA-induced disturbance testified BBR regulating dysfunction, podocyte apoptosis glomerulopathy progression DKD.Results: Intragastric administration for 8 weeks significantly reversed glucose lipid metabolism disorders, damage, basement membrane thickening, mesangial expansion glomerulosclerosis.BBR strongly inhibited apoptosis, increased reactive oxygen species (ROS) generation, fragmentation dysfunction both vivo vitro.Mechanistically, could stabilize morphology via abolishing palmitic (PA)-induced activation dynamin-related protein 1 (Drp1).Conclusions: Our study demonstrated first time that may have a previously unrecognized role protecting glomerulus positively Drp1-mediated dynamics.It might serve as novel therapeutic drug treatment DKD.

Язык: Английский

Процитировано

154

Pathophysiology of AKI to CKD progression DOI
Yuki Sato, Masahiro Takahashi, Motoko Yanagita

и другие.

Seminars in Nephrology, Год журнала: 2020, Номер 40(2), С. 206 - 215

Опубликована: Март 1, 2020

Язык: Английский

Процитировано

153

Mitochondrial dysfunction and the AKI-to-CKD transition DOI
Mingzhu Jiang, Mi Bai, Juan Lei

и другие.

AJP Renal Physiology, Год журнала: 2020, Номер 319(6), С. F1105 - F1116

Опубликована: Окт. 19, 2020

Acute kidney injury (AKI) has been widely recognized as an important risk factor for the occurrence and development of chronic disease (CKD). Even milder AKI adverse consequences could progress to renal fibrosis, which is ultimate common pathway various terminal diseases. Thus, it urgent develop a strategy hinder transition from CKD. Some mechanisms AKI-to-CKD have revealed, such nephron loss, cell cycle arrest, persistent inflammation, endothelial with vascular rarefaction, epigenetic changes. Previous studies elucidated pivotal role mitochondria in acute injuries demonstrated that fitness this organelle major determinant both pathogenesis recovery organ function. Recent research suggested damage mitochondrial function early crucial leading tubular insufficiency. Dysregulation homeostasis, alterations bioenergetics, stress cross talk contribute transition. In review, we focus on pathophysiology after progression CKD, confirming targeting represents potentially effective therapeutic

Язык: Английский

Процитировано

150