The potential roles of galectin-3 in AKI and CKD

被引：12

作者：

Wang, Fengyun ^{[1
]}

Zhou, Lixin ^{[2
]}

Eliaz, Amity ^{[3
]}

Hu, Chang ^{[1
]}

Qiang, Xinhua ^{[2
]}

Ke, Li ^{[1
]}

Chertow, Glenn ^{[3
]}

Eliaz, Isaac ^{[4
]}

Peng, Zhiyong ^{[1
,5
]}

机构：

[1] Wuhan Univ, Zhongnan Hosp, Dept Crit Care Med, Wuhan, Hubei, Peoples R China

[2] First Peoples Hosp Foshan, Dept Crit Care Med, Foshan, Peoples R China

[3] Stanford Univ, Dept Med, Sch Med, Stanford, CA USA

[4] Amitabha Med Ctr, Santa Rosa, CA 95401 USA

[5] Univ Pittsburgh, Ctr Crit Care Nephrol, Dept Crit Care Med, Med Ctr, Pittsburgh, PA 15260 USA

来源：

FRONTIERS IN PHYSIOLOGY | 2023年 / 14卷

基金：

中国国家自然科学基金;

关键词：

acute kidney injury; chronic kidney disease; inflammation; galectin-3; renal fibrosis; ACUTE KIDNEY INJURY; PHARMACOLOGICAL INHIBITION; EXPRESSION; BIOMARKER; ISCHEMIA; DAMAGE; ASSOCIATION; PROTECTS; FIBROSIS; FAILURE;

D O I：

10.3389/fphys.2023.1090724

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

Acute kidney injury (AKI) is a common condition with high morbidity and mortality, and is associated with the development and progression of chronic kidney disease (CKD). The beta-galactoside binding protein galectin-3 (Gal3), with its proinflammatory and profibrotic properties, has been implicated in the development of both AKI and CKD. Serum Gal3 levels are elevated in patients with AKI and CKD, and elevated Gal3 is associated with progression of CKD. In addition, Gal3 is associated with the incidence of AKI among critically ill patients, and blocking Gal3 in murine models of sepsis and ischemia-reperfusion injury results in significantly lower AKI incidence and mortality. Here we review the role of Gal3 in the pathophysiology of AKI and CKD, as well as the therapeutic potential of targeting Gal3.

引用

页数：7

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