Heart failure (HF) is a complex syndrome and a leading cause of mortality worldwide. While current medical treatment is based on known pathophysiology and is effective for many patients, the underlying cellular mechanisms are poorly understood. Energy deficiency is a characteristic of HF, marked by complex alterations in metabolism. Within the tricarboxylic acid cycle, anaplerosis emerges as an essential metabolic process responsible for replenishing lost intermediates, thereby playing a crucial role in sustaining energy metabolism and consequently cardiac function. Alterations in cardiac anaplerosis are commonly observed in HF, demonstrating potential for therapeutic intervention. This review discusses recent advances in understanding the anaplerotic adaptations that occur in HF. We also explore therapeutics that can directly modulate anaplerosis or are likely to confer cardioprotective effects through anaplerosis, which could potentially be implemented to rescue the failing heart.

中文翻译：

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心力衰竭的过敏性填充：机制和潜在治疗综述


心力衰竭 （HF） 是一种复杂的综合征，也是全球死亡的主要原因。虽然目前的医学治疗基于已知的病理生理学并且对许多患者有效，但对潜在的细胞机制知之甚少。能量缺乏是 HF 的一个特征，以新陈代谢的复杂改变为特征。在三羧酸循环中，厌氧反应成为一种重要的代谢过程，负责补充丢失的中间体，从而在维持能量代谢和心脏功能方面起着至关重要的作用。在 HF 中常见观察到心脏吻合的改变，表明具有治疗干预的潜力。本综述讨论了理解 HF 中发生的厌氧适应的最新进展。我们还探索了可以直接调节吻合作用或可能通过吻合作用赋予心脏保护作用的疗法，这些疗法有可能用于挽救衰竭的心脏。