Cargando…
The KCa3.1 blocker TRAM34 reverses renal damage in a mouse model of established diabetic nephropathy
Despite optimal control of hyperglycaemia, hypertension, and dyslipidaemia, the number of patients with diabetic nephropathy (DN) continues to grow. Strategies to target various signaling pathways to prevent DN have been intensively investigated in animal models and many have been proved to be promi...
Autores principales: | Huang, Chunling, Zhang, Ling, Shi, Ying, Yi, Hao, Zhao, Yongli, Chen, Jason, Pollock, Carol A., Chen, Xin-Ming |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5806905/ https://www.ncbi.nlm.nih.gov/pubmed/29425253 http://dx.doi.org/10.1371/journal.pone.0192800 |
Ejemplares similares
-
KCa3.1 mediates activation of fibroblasts in diabetic renal interstitial fibrosis
por: Huang, Chunling, et al.
Publicado: (2014) -
Blockade of KCa3.1 Ameliorates Renal Fibrosis Through the TGF-β1/Smad Pathway in Diabetic Mice
por: Huang, Chunling, et al.
Publicado: (2013) -
High Glucose Induces CCL20 in Proximal Tubular Cells via Activation of the KCa3.1 Channel
por: Huang, Chunling, et al.
Publicado: (2014) -
KCa3.1 Mediates Dysregulation of Mitochondrial Quality Control in Diabetic Kidney Disease
por: Huang, Chunling, et al.
Publicado: (2021) -
KCa3.1 mediates dysfunction of tubular autophagy in diabetic kidneys via PI3k/Akt/mTOR signaling pathways
por: Huang, Chunling, et al.
Publicado: (2016)