Mitogen-Activated Protein Kinases and Hypoxic/Ischemic Nephropathy
- PMID: 27544204
- DOI: 10.1159/000447812
Mitogen-Activated Protein Kinases and Hypoxic/Ischemic Nephropathy
Abstract
Tissue hypoxia/ischemia is a pathological feature of many human disorders including stroke, myocardial infarction, hypoxic/ischemic nephropathy, as well as cancer. In the kidney, the combination of limited oxygen supply to the tissues and high oxygen demand is considered the main reason for the susceptibility of the kidney to hypoxic/ischemic injury. In recent years, increasing evidence has indicated that a reduction in renal oxygen tension/blood supply plays an important role in acute kidney injury, chronic kidney disease, and renal tumorigenesis. However, the underlying signaling mechanisms, whereby hypoxia alters cellular behaviors, remain poorly understood. Mitogen-activated protein kinases (MAPKs) are key signal-transducing enzymes activated by a wide range of extracellular stimuli, including hypoxia/ischemia. There are four major family members of MAPKs: the extracellular signal-regulated kinases-1 and -2 (ERK1/2), the c-Jun N-terminal kinases (JNK), p38 MAPKs, and extracellular signal-regulated kinase-5 (ERK5/BMK1). Recent studies, including ours, suggest that these MAPKs are differentially involved in renal responses to hypoxic/ischemic stress. This review will discuss their changes in hypoxic/ischemic pathophysiology with acute kidney injury, chronic kidney diseases and renal carcinoma.
© 2016 The Author(s) Published by S. Karger AG, Basel.
Similar articles
-
Mitogen-activated protein kinases in the porcine retinal arteries and neuroretina following retinal ischemia-reperfusion.Mol Vis. 2010 Mar 10;16:392-407. Mol Vis. 2010. PMID: 20300568 Free PMC article.
-
DUSP6 (MKP3) null mice show enhanced ERK1/2 phosphorylation at baseline and increased myocyte proliferation in the heart affecting disease susceptibility.J Biol Chem. 2008 Nov 7;283(45):31246-55. doi: 10.1074/jbc.M806085200. Epub 2008 Aug 27. J Biol Chem. 2008. PMID: 18753132 Free PMC article.
-
Ischemic preconditioning improved renal ischemia/reperfusion injury and hyperglycemia.IUBMB Life. 2019 Mar;71(3):321-329. doi: 10.1002/iub.1972. Epub 2018 Nov 27. IUBMB Life. 2019. PMID: 30481400
-
The role of stress-activated protein kinase signaling in renal pathophysiology.Braz J Med Biol Res. 2009 Jan;42(1):29-37. doi: 10.1590/s0100-879x2008005000049. Epub 2008 Nov 7. Braz J Med Biol Res. 2009. PMID: 18982195 Review.
-
Impact of Conventional and Atypical MAPKs on the Development of Metabolic Diseases.Biomolecules. 2020 Aug 29;10(9):1256. doi: 10.3390/biom10091256. Biomolecules. 2020. PMID: 32872540 Free PMC article. Review.
Cited by
-
c-Jun N-Terminal Kinases (JNKs) in Myocardial and Cerebral Ischemia/Reperfusion Injury.Front Pharmacol. 2018 Jul 5;9:715. doi: 10.3389/fphar.2018.00715. eCollection 2018. Front Pharmacol. 2018. PMID: 30026697 Free PMC article. Review.
-
Insights into the effects of apelin-13 on renal function and NHE3 activity following ischemia/reperfusion-induced acute kidney injury.Front Physiol. 2025 Mar 19;16:1544274. doi: 10.3389/fphys.2025.1544274. eCollection 2025. Front Physiol. 2025. PMID: 40177358 Free PMC article.
-
The Effect of Low-Density Lipoprotein Receptor-Related Protein-1 on Acute Kidney Injury and Renal Tubular Epithelial Triglyceride Accumulation.Kidney Dis (Basel). 2025 Apr 14;11(1):320-331. doi: 10.1159/000545851. eCollection 2025 Jan-Dec. Kidney Dis (Basel). 2025. PMID: 40432903 Free PMC article.
-
Carnosol protects against renal ischemia-reperfusion injury in rats.Exp Anim. 2018 Nov 1;67(4):545-553. doi: 10.1538/expanim.18-0067. Epub 2018 Jul 31. Exp Anim. 2018. PMID: 30068825 Free PMC article.
-
Mesna ameliorates acute lung injury induced by intestinal ischemia-reperfusion in rats.Sci Rep. 2021 Jun 25;11(1):13356. doi: 10.1038/s41598-021-92653-7. Sci Rep. 2021. PMID: 34172794 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Research Materials
Miscellaneous