Cargando…
High Glucose Induces CCL20 in Proximal Tubular Cells via Activation of the KCa3.1 Channel
BACKGROUND: Inflammation plays a key role in the development and progression of diabetic nephropathy (DN). KCa3.1, a calcium activated potassium channel protein, is associated with vascular inflammation, atherogenesis, and proliferation of endothelial cells, macrophages, and fibroblasts. We have pre...
Autores principales: | Huang, Chunling, Pollock, Carol A., Chen, Xin-Ming |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2014
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986377/ https://www.ncbi.nlm.nih.gov/pubmed/24733189 http://dx.doi.org/10.1371/journal.pone.0095173 |
Ejemplares similares
-
KCa3.1 mediates dysfunction of tubular autophagy in diabetic kidneys via PI3k/Akt/mTOR signaling pathways
por: Huang, Chunling, et al.
Publicado: (2016) -
KCa3.1 mediates activation of fibroblasts in diabetic renal interstitial fibrosis
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) -
Contribution of the KCa3.1 channel–calmodulin interactions to the regulation of the KCa3.1 gating process
por: Morales, Patricia, et al.
Publicado: (2013) -
Blockade of KCa3.1 Ameliorates Renal Fibrosis Through the TGF-β1/Smad Pathway in Diabetic Mice
por: Huang, Chunling, et al.
Publicado: (2013)