Abstract
Cardiac hypertrophy, a stereotypic cardiac response to increased workload, ultimately progresses to severe contractile dysfunction and uncompensated heart failure without appropriate intervention. Sustained cardiac overload inevitably results in high energy consumption, thus breaking the balance between mitochondrial energy supply and cardiac energy demand. In recent years, accumulating evidence has indicated that mitochondrial dysfunction is implicated in pathological cardiac hypertrophy. The significant alterations in mitochondrial energetics and mitochondrial proteome composition, as well as the altered expression of transcripts that have an impact on mitochondrial structure and function, may contribute to the initiation and progression of cardiac hypertrophy. This article presents a summary review of the morphological and functional changes of mitochondria during the hypertrophic response, followed by an overview of the latest research progress on the significant modulatory roles of mitochondria in cardiac hypertrophy. Our article is also to summarize the strategies of mitochondria-targeting as therapeutic targets to treat cardiac hypertrophy.
Highlights
Cardiomyocytes (CMs) are one of the most important cell types which become terminally differentiated once after birth
Mitochondria are the prominent organelle for the energy supply of CMs, and a large number of researches have demonstrated that mitochondria are highly susceptible to pathological stimuli, including sustained and repeated cardiac overload [5, 16]
Efficient cardiac therapies targeting mitochondrial lesions and dysfunction may constitute a new strategy to inhibit the high susceptibility to pro-hypertrophic stimuli and attenuate pathological cardiac hypertrophy (Table 2)
Summary
Dan Yang , 1,2† Han-Qing Liu 3†, Fang-Yuan Liu 1,2, Zhen Guo 1,2, Peng An 1,2, Ming-Yu Wang 1,2, Zheng Yang 1,2, Di Fan 1,2* and Qi-Zhu Tang 1,2*. A stereotypic cardiac response to increased workload, progresses to severe contractile dysfunction and uncompensated heart failure without appropriate intervention. In recent years, accumulating evidence has indicated that mitochondrial dysfunction is implicated in pathological cardiac hypertrophy. The significant alterations in mitochondrial energetics and mitochondrial proteome composition, as well as the altered expression of transcripts that have an impact on mitochondrial structure and function, may contribute to the initiation and progression of cardiac hypertrophy. This article presents a summary review of the morphological and functional changes of mitochondria during the hypertrophic response, followed by an overview of the latest research progress on the significant modulatory roles of mitochondria in cardiac hypertrophy. Our article is to summarize the strategies of mitochondria-targeting as therapeutic targets to treat cardiac hypertrophy
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