☆ 4.7 Article

Renalase regulates renal tubular injury in diabetic nephropathy via the p38MAPK signaling pathway

FASEB JOURNAL (2023)

相关参考文献

注意：仅列出部分参考文献，下载原文获取全部文献信息。

Article Biochemistry & Molecular Biology

Empagliflozin attenuates the renal tubular ferroptosis in diabetic kidney disease through AMPK/NRF2 pathway

QianYu Lu et al.

Summary: Renal tubular damage is a key factor in the development of diabetic kidney disease (DKD), with ferroptosis as the main pathological process. Empagliflozin has been suggested as a potential treatment for renal injury, but its effects on diabetic-related ferroptosis and underlying mechanisms are not fully understood. This study evaluated the influence of empagliflozin on renal injury using mouse models and cell lines, and found that it can decrease ferroptosis in DKD mice and high-glucose stimulated cells. The protective effects of empagliflozin are partially mediated by AMP-activated protein kinase (AMPK) and the NRF2 activation pathway. These findings offer important insights for novel treatment approaches for DKD.

FREE RADICAL BIOLOGY AND MEDICINE (2023)

添加到收藏夹

Review Endocrinology & Metabolism

Role of renal tubular programed cell death in diabetic kidney disease

Xiaojun Zhou et al.

Summary: The pathogenic mechanism of DKD involves various functions, but its inadequate characterization limits effective treatments. Tubular damage is closely related to renal function and is considered the main contributor to early DKD injury. Programed cell death plays a crucial role in DKD pathogenesis, and various types of cell death, including classical apoptosis, autophagic cell death, and pyroptosis, have been studied extensively. This review aims to elucidate the current understanding of the mechanism of DKD and explore the therapeutic potential of drugs targeting tubular cell death pathways.

DIABETES-METABOLISM RESEARCH AND REVIEWS (2023)

添加到收藏夹

Review Medicine, Research & Experimental

Molecular pathways that drive diabetic kidney disease

Samer Mohandes et al.

Summary: Kidney disease is a leading cause of death in diabetes patients, with diabetic kidney disease (DKD) accounting for nearly half of all chronic kidney disease cases. Podocytes and endothelial cells are found to play a crucial role in the development of albuminuria and early kidney disease in diabetes. Hyperglycemia induces cellular stress in the kidney, leading to changes in cellular metabolism and an excessive workload for proximal tubule cells. Later, mitochondrial defects result in increased oxidative stress and activation of inflammatory pathways, causing progressive decline in kidney function and fibrosis. Blocking the renin-angiotensin system or the sodium-glucose cotransporter can protect cells and slow down the decline in kidney function. Newly identified molecular pathways may pave the way for the development of much-needed novel therapeutics.

JOURNAL OF CLINICAL INVESTIGATION (2023)

添加到收藏夹

Article Urology & Nephrology

CKD in China: Evolving Spectrum and Public Health Implications

Chao Yang et al.

AMERICAN JOURNAL OF KIDNEY DISEASES (2020)

添加到收藏夹

Article Medicine, Research & Experimental

A protective role of renalase in diabetic nephropathy

Jianyong Yin et al.

CLINICAL SCIENCE (2020)

添加到收藏夹

Article Urology & Nephrology

Novel tubular-glomerular interplay in diabetic kidney disease mediated by sirtuin 1, nicotinamide mononucleotide, and nicotinamide adenine dinucleotide Oshima Award Address 2017

Kazuhiro Hasegawa

CLINICAL AND EXPERIMENTAL NEPHROLOGY (2019)

添加到收藏夹

Review Urology & Nephrology

Renal tubule injury: a driving force toward chronic kidney disease

Bi-Cheng Liu et al.

KIDNEY INTERNATIONAL (2018)

添加到收藏夹

Article Biochemistry & Molecular Biology

Renalase Protects against Renal Fibrosis by Inhibiting the Activation of the ERK Signaling Pathways

Yiru Wu et al.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2017)

添加到收藏夹

Review Cell Biology

Extracellular renalase protects cells and organs by outside-in signalling

Yang Wang et al.

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE (2017)

添加到收藏夹

Article Urology & Nephrology

The genetic architecture of DKD in T1DM

Ellen F. Carney

Nature Reviews Nephrology (2016)

添加到收藏夹

Article Urology & Nephrology

Renalase Prevents AKI Independent of Amine Oxidase Activity

Ling Wang et al.

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY (2014)

添加到收藏夹

Article Urology & Nephrology

Renalase Protects against Ischemic AKI

H. Thomas Lee et al.

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY (2013)

添加到收藏夹

Letter Urology & Nephrology

Does renalase degrade catecholamines?

Nina Eikelis et al.

KIDNEY INTERNATIONAL (2011)

添加到收藏夹

Article Physiology

p66Shc mediates high-glucose and angiotensin II-induced oxidative stress renal tubular injury via mitochondrial-dependent apoptotic pathway

Lin Sun et al.

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY (2010)

添加到收藏夹

Article Physiology

Interplay between Akt and p38 MAPK pathways in the regulation of renal tubular cell apoptosis associated with diabetic nephropathy

Madhavi J. Rane et al.

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY (2010)

添加到收藏夹

Article Urology & Nephrology

TGF-β concentration specifies differential signaling profiles of growth arrest/differentiation land apoptosis in podocytes

DT Wu et al.

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY (2005)

添加到收藏夹

Article Physiology

ERK and p38 mediate high-glucose-induced hypertrophy and TGF-beta expression in renal tubular cells

H Fujita et al.

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY (2004)

添加到收藏夹

© Peeref 2019-2024. All rights reserved.