Arjamaa Olli
University of Turku Biodiversity Unit, Turku, Finland
Open Heart. 2025 Mar 22;12(1):e003130. doi: 10.1136/openhrt-2024-003130.
Mechanical stress on the heart is commonly considered the sole stimulus explaining the synthesis and release of circulating natriuretic peptides and their derivatives. While one of the most critical paradigms in cardiology is that mechanical load increases oxygen consumption, clinical studies on these peptides have neglected the relationship between mechanical stress and oxygen metabolism. At the cellular level, cardiac myocytes have a ubiquitous oxygen-sensing pathway mediated by a nuclear transcription factor, the hypoxia-inducible factor (HIF). Published studies indicate that the human myocardium starts expressing HIF during infarction. In myocardial cell cultures, natriuretic peptides are synthesised and released under hypoxic conditions through immediate and sufficient actions of HIF.
Myocardial oxygen metabolism directly regulates the plasma levels of natriuretic peptides in heart diseases. The function of oxygen gradients should be correlated with circulating natriuretic peptides to achieve better sensitivity in plasma measurements of natriuretic peptides in myocardial infarction.
心脏的机械应力通常被认为是解释循环利钠肽及其衍生物合成与释放的唯一刺激因素。虽然心脏病学中最关键的范例之一是机械负荷会增加氧消耗，但关于这些肽的临床研究却忽略了机械应力与氧代谢之间的关系。在细胞水平上，心肌细胞具有由核转录因子缺氧诱导因子（HIF）介导的普遍存在的氧感应途径。已发表的研究表明，人类心肌在梗死期间开始表达HIF。在心肌细胞培养中，利钠肽在缺氧条件下通过HIF的即时和充分作用而合成并释放。
心肌氧代谢直接调节心脏病中利钠肽的血浆水平。氧梯度的功能应与循环利钠肽相关联，以在心肌梗死中利钠肽的血浆测量中获得更好的灵敏度。
