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Metabolic remodeling induced by mitokines in heart failure
被引:12
|作者:
Duan, Jiahao
[1
]
Chen, Zijun
[1
]
Wu, Yeshun
[1
]
Zhu, Bin
[2
]
Yang, Ling
[1
]
Yang, Chun
[3
]
机构:
[1] Soochow Univ, Dept Cardiol, Affiliated Hosp 3, Changzhou 213003, Peoples R China
[2] Soochow Univ, Dept Crit Care Med, Affiliated Hosp 3, Changzhou 213003, Peoples R China
[3] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Anesthesiol, Wuhan 430030, Hubei, Peoples R China
来源:
基金:
中国国家自然科学基金;
关键词:
heart;
metabolism;
mitohormesis;
peptides;
retrograde signaling;
GROWTH-FACTOR;
21;
UNFOLDED PROTEIN RESPONSE;
BODY-MASS INDEX;
DIFFERENTIATION FACTOR 15;
INDUCED CARDIAC-HYPERTROPHY;
BETA-KLOTHO EXPRESSION;
OXIDATIVE STRESS;
MOTS-C;
ENERGY-METABOLISM;
DOWN-REGULATION;
D O I:
10.18632/aging.102247
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
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 mitochondria! 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.
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页码:7307 / 7327
页数:21
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