Cargando…
Succinate induces aberrant mitochondrial fission in cardiomyocytes through GPR91 signaling
Altered mitochondrial metabolism acts as an initial cause for cardiovascular diseases and metabolic intermediate succinate emerges as a mediator of mitochondrial dysfunction. This work aims to investigate whether or not extracellular succinate accumulation and its targeted G protein-coupled receptor...
Autores principales: | Lu, Yi-Tong, Li, Lan-Zhu, Yang, Yi-Lin, Yin, Xiaojian, Liu, Qun, Zhang, Lei, Liu, Kang, Liu, Baolin, Li, Jia, Qi, Lian-Wen |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986788/ https://www.ncbi.nlm.nih.gov/pubmed/29867110 http://dx.doi.org/10.1038/s41419-018-0708-5 |
Ejemplares similares
-
Succinate causes pathological cardiomyocyte hypertrophy through GPR91 activation
por: Aguiar, Carla J, et al.
Publicado: (2014) -
Succinate promotes stem cell migration through the GPR91-dependent regulation of DRP1-mediated mitochondrial fission
por: Ko, So Hee, et al.
Publicado: (2017) -
Author Correction: Succinate promotes stem cell migration through the GPR91-dependent regulation of DRP1-mediated mitochondrial fission
por: Ko, So Hee, et al.
Publicado: (2018) -
The Succinate Receptor GPR91 Is Involved in Pressure Overload-Induced Ventricular Hypertrophy
por: Yang, Lei, et al.
Publicado: (2016) -
Receptor structure-based discovery of non-metabolite agonists for the succinate receptor GPR91
por: Trauelsen, Mette, et al.
Publicado: (2017)