Signal pathways involved in contrast-induced acute kidney injury DOI Creative Commons
Ke Deng,

Mingxin Pei,

Beibei Li

et al.

Frontiers in Physiology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 25, 2024

Contrast-induced acute kidney injury (CI-AKI) has emerged as a global public health concern, ranking the third most prevalent cause of hospital-acquired injury, which is related to adverse outcomes. However, its precise pathogenesis remains elusive. Consequently, researchers are dedicated uncovering CI-AKI's pathophysiology and signaling pathways, including inflammation, oxidative stress, apoptosis, ferroptosis, improve prevention treatment. This review thoroughly analyzes pathways their interactions associated with CI-AKI, assesses impact various research models on pathway analysis, explores more targeted treatment approaches. Aims furnish robust theoretical foundation for molecular mechanisms underpinning clinical treatments.

Language: Английский

p16INK4a Aggravated Sepsis-associated Cardiac Injury by Inhibiting the PI3K/AKT Pathway and Inducing Redox Imbalance DOI
Baihong Li, Wei Wang, Xiaoyan Wang

et al.

Journal of Cardiovascular Translational Research, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 14, 2025

Language: Английский

Citations

0
p16INK4a promoted progress of MCT induced pulmonary hypertension via maintaining redox balance and autophagy pathway DOI
Fen Wang, Xiao Wang, Jianwei Li

et al.

Biochemical and Biophysical Research Communications, Journal Year: 2025, Volume and Issue: 749, P. 151385 - 151385

Published: Jan. 23, 2025

Language: Английский

Citations

0
p16INK4a Deletion Alleviated Obesity‐Associated Kidney Fibrosis by Regulating Metabolic Reprogramming and the Inflammasome Pathway DOI Creative Commons
Jun Li, Fen Wang,

Yuan Du

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2025, Volume and Issue: 29(5)

Published: March 1, 2025

ABSTRACT Recent research has revealed a close association between obesity and various metabolic disorders, including renal diseases, but the mechanism is still unknown. This study explored role of p16INK4a in obesity‐related kidney fibrosis evaluated its potential as therapeutic target. Using wild‐type (WT) mice p16 KO mice, we fed both groups high‐fat diet (HFD) for 6 months. Our results showed that an HFD led to significant weight gain increased expression WT mouse kidneys. Notably, presented reduced fibrosis, indicated by decreased levels profibrotic proteins (α‐SMA collagen I) improved histological outcomes, glomeruli tubules. P16 also suppressed several proinflammatory biomarkers (MMP1, MMP3, IL‐1β, TNF‐α IL‐6) inhibited NLRP3 inflammasome pathway. The administration ABT263 further validated these findings decreasing inflammation HFD‐fed suggesting contributes fibrotic inflammatory processes. Metabolomic analyses knockout influenced pathways, linoleic acid pyrimidine metabolism, HFD‐induced Additionally, over‐expression was observed kidneys chronic disease patients with long‐term hyperlipidaemia. These highlight critical obesity‐induced damage suggest targeting may be promising approach treating inflammation.

Language: Английский

Citations

0
Baicalin reduced vandetanib induced myocardial injury by regulating redox balance and NLRP3 inflammasome pathway DOI
Fen Wang, Jianwei Li, Zhixuan Zhang

et al.

Tissue and Cell, Journal Year: 2025, Volume and Issue: 94, P. 102795 - 102795

Published: Feb. 16, 2025

Language: Английский

Citations

0
Cellular senescence in acute kidney injury: Target and opportunity DOI
Ting Li, Kexin Yang, Wei Gao

et al.

Biochemical and Biophysical Research Communications, Journal Year: 2024, Volume and Issue: 706, P. 149744 - 149744

Published: March 7, 2024

Language: Английский

Citations

1
Signal pathways involved in contrast-induced acute kidney injury DOI Creative Commons
Ke Deng,

Mingxin Pei,

Beibei Li

et al.

Frontiers in Physiology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 25, 2024

Contrast-induced acute kidney injury (CI-AKI) has emerged as a global public health concern, ranking the third most prevalent cause of hospital-acquired injury, which is related to adverse outcomes. However, its precise pathogenesis remains elusive. Consequently, researchers are dedicated uncovering CI-AKI's pathophysiology and signaling pathways, including inflammation, oxidative stress, apoptosis, ferroptosis, improve prevention treatment. This review thoroughly analyzes pathways their interactions associated with CI-AKI, assesses impact various research models on pathway analysis, explores more targeted treatment approaches. Aims furnish robust theoretical foundation for molecular mechanisms underpinning clinical treatments.

Language: Английский

Citations

0