Unknown

Dataset Information

0

Metabolic remodeling induced by mitokines in heart failure.


ABSTRACT: The prevalence rates of heart failure (HF) are greater than 10% in individuals aged >75 years, indicating an intrinsic link between aging and HF. It has been recognized that mitochondrial dysfunction contributes to the pathology of HF. Mitokines are a type of cytokines, peptides, or signaling pathways produced or activated by the nucleus or the mitochondria through cell non-autonomous responses during cellular stress. In addition to promoting the communication between the mitochondria and the nucleus, mitokines also exert a systemic regulatory effect by circulating to distant tissues. It is noteworthy that increasing evidence has demonstrated that mitokines are capable of reducing the metabolic-related HF risk factors and are associated with HF severity. Consequently, mitokines might represent a potential therapy target for HF.

SUBMITTER: Duan J 

PROVIDER: S-EPMC6756899 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

altmetric image

Publications

Metabolic remodeling induced by mitokines in heart failure.

Duan Jiahao J   Chen Zijun Z   Wu Yeshun Y   Zhu Bin B   Yang Ling L   Yang Chun C  

Aging 20190909 17


The prevalence rates of heart failure (HF) are greater than 10% in individuals aged >75 years, indicating an intrinsic link between aging and HF. It has been recognized that mitochondrial dysfunction contributes to the pathology of HF. Mitokines are a type of cytokines, peptides, or signaling pathways produced or activated by the nucleus or the mitochondria through cell non-autonomous responses during cellular stress. In addition to promoting the communication between the mitochondria and the nu  ...[more]

Similar Datasets

| S-EPMC4366225 | biostudies-literature
| S-EPMC7645995 | biostudies-literature
| S-EPMC4934852 | biostudies-literature
| S-EPMC5341031 | biostudies-literature
| S-EPMC5490953 | biostudies-other
| S-EPMC9894375 | biostudies-literature
| S-EPMC4075482 | biostudies-literature
| S-EPMC8745344 | biostudies-literature
| S-EPMC4206603 | biostudies-literature
| S-EPMC5879679 | biostudies-literature