期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 161, 期 -, 页码 106-115出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2021.08.003
关键词
Sodium; Cardiac metabolism; Heart failure; Sodium pump; Energetics
资金
- British Heart Foundation Accelerator Award [AA/18/5/34222]
- Diabetes UK Grant [19/0005973]
- Barts Charity Grant [MRC 0215]
- Wellcome Trust [221604/Z/20/Z]
- British Heart Foundation [RG/12/4/29426]
- Wellcome Trust [221604/Z/20/Z] Funding Source: Wellcome Trust
Elevated intracellular sodium and metabolic impairment are common features of heart failure. Studies have shown that sodium elevation affects mitochondrial function, providing important insights into the pathophysiology of heart failure and potential treatment strategies.
Elevated intracellular Na (Nai) and metabolic impairment are interrelated pathophysiological features of the failing heart (HF). There have been a number of studies showing that myocardial sodium elevation subtly affects mitochondrial function. During contraction, mitochondrial calcium (Camito) stimulates a variety of TCA cycle enzymes, thereby providing reducing equivalents to maintain ATP supply. Nai elevation has been shown to impact Camito; however, whether metabolic remodelling in HF is caused by increased Nai has only been recently demonstrated. This novel insight may help to elucidate the contribution of metabolic remodelling in the pathophysiology of HF, the lack of efficacy of current HF therapies and a rationale for the development of future metabolism-targeting treatments. Here we review the relationship between Na pump inhibition, elevated Nai, and altered metabolic profile in the context of HF and their link to metabolic (in)flexibility and mitochondrial reprogramming.
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