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Published on: August 9, 2013
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MAP3K kinases and kidney injury
Leticia Cuarental1, David Sucunza-Sáenz2, Lara Valiño-Rivas1
1IIS-Fundacion Jimenez Diaz-UAM, Madrid, Spain; REDINREN, Spain.
Nefrologia
|June 15, 2019
Summary
Mitogen-activated protein kinase kinase kinases (MAP3Ks) are crucial upstream regulators in kidney disease. Some MAP3Ks show therapeutic potential, but most remain unexplored in kidney injury.
Area of Science:
- Cellular signaling pathways
- Renal pathophysiology
- Kinase biology
Background:
- Mitogen-activated protein kinases (MAPKs) regulate kidney cell survival, death, differentiation, and proliferation.
- MAPK signaling involves a cascade of three kinases: MAP3K, MAP2K, and MAPK.
- While MAPKs are well-studied in kidney injury, the role of upstream MAP3Ks is less understood.
Purpose of the Study:
- To review the involvement of MAP3Ks in non-malignant kidney disease.
- To explore available therapeutic tools targeting MAP3Ks in kidney disease.
- To highlight the potential of MAP3Ks as therapeutic targets in kidney injury.
Main Methods:
- Literature review of current knowledge on MAP3K involvement in kidney disease.
- Analysis of in vivo interventional evidence for specific MAP3Ks.
- Examination of therapeutic strategies and clinical trial data for MAP3K inhibitors.
Main Results:
- MAP3K5 (ASK1) and MAP3K14 (NIK) are implicated in experimental kidney disease pathogenesis.
- MAP3K7 (MEKK7) inhibition protected against acute and chronic kidney injury.
- MAP3K8 (TPL2/Cot) inhibition protected against acute kidney injury; MAP3K15 (ASK3) may protect against hypertension.
- BRAF inhibitors can induce acute kidney injury and nephrotic syndrome.
Conclusions:
- MAP3Ks are upstream regulators of intracellular signaling and potential therapeutic targets in kidney injury.
- Evidence supports the role of specific MAP3Ks (e.g., ASK1, NIK, MEKK7) in kidney disease.
- The roles of most MAP3Ks in kidney disease remain largely unexplored, necessitating further research.
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