Mitogen-Activated Protein Kinases and Hypoxic/Ischemic Nephropathy

@article{Luo2016MitogenActivatedPK,
  title={Mitogen-Activated Protein Kinases and Hypoxic/Ischemic Nephropathy},
  author={Fengbao Luo and Jian-Ting Shi and Qianqian Shi and Xianlin Xu and Ying Xia and Xiaozhou He},
  journal={Cellular Physiology and Biochemistry},
  year={2016},
  volume={39},
  pages={1051 - 1067}
}
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… 

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References

SHOWING 1-10 OF 155 REFERENCES

The role of stress-activated protein kinase signaling in renal pathophysiology.

  • F. MaJ. LiuD. Nikolic-Paterson
  • Biology, Medicine
    Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • 2009
TLDR
Administration of small molecule inhibitors of p38 and JNK has been shown to provide protection from renal injury in different types of experimental kidney disease through inhibition of renal inflammation, fibrosis, and apoptosis.

MAPK activation determines renal epithelial cell survival during oxidative injury.

TLDR
It is indicated that cell survival in the kidney after ischemia may be dependent on ERK activation, suggesting that this pathway may be a target for therapeutic treatment in I/R injury.

Mitogen activated protein kinases in renal fibrosis.

TLDR
Administration of specific inhibitors of individual MAP kinases has identified a pathogenic role for both p38 and JNK pathways in animal models of renal fibrosis, and evidence to suggest that MAPKinase kinases are activated in human kidney fibrosis.

Compromised MAPK signaling in human diseases: an update

TLDR
Recent research on the roles of MAPK signaling pathways in human diseases, with a focus on cancer and neurodegenerative conditions is summarized.

A Death-Promoting Role for Extracellular Signal-Regulated Kinase

TLDR
The evidence and mechanism of ERK-induced apoptosis in both cell culture and in animal models is summarized.

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

TLDR
The current insights into oxygen transport pathways, from oxygen supply to oxygen consumption in the kidney and from the adaptation mechanisms to renal hypoxia, are reviewed to place oxygen pathways’ alterations as a potential central player in the pathogenesis of acute kidney injury.

The Role of p38α Mitogen-Activated Protein Kinase Activation in Renal Fibrosis

TLDR
It is demonstrated that p38alpha MAPK plays an important role in renal fibrosis, acting downstream of TGF-beta1, and blockade of p38 MAPK reduces extracellular matrix production and may be considered a potential therapeutic option in the treatment of kidney fibrosis.

The protein kinase 2 inhibitor tetrabromobenzotriazole protects against renal ischemia reperfusion injury

TLDR
Results suggest that CK2 α mediates proapoptotic and proinflammatory signaling, thus the CK2α inhibitor may be used to prevent renal I/R injuries observed in clinical settings.

Mammalian mitogen-activated protein kinase signal transduction pathways activated by stress and inflammation.

TLDR
This review focuses on the biochemical components and regulation of mammalian stress-regulated mitogen-activated protein kinase (MAPK) pathways, and the nuclear factor-kappa B pathway, a second stress signaling paradigm.

The role of p38alpha mitogen-activated protein kinase activation in renal fibrosis.

TLDR
It is demonstrated that p38alpha MAPK plays an important role in renal fibrosis, acting downstream of TGF-beta1, and blockade of p38 MAPK reduces extracellular matrix production and may be considered a potential therapeutic option in the treatment of kidney fibrosis.
...