Marelli-Berg Federica M, Aksentijevic Dunja
William Harvey Research Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Centre for Inflammation and Therapeutic Innovation, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Cell Stress. 2019 Jun 7;3(8):240-266. doi: 10.15698/cst2019.08.194.
Inflammatory processes underlie many diseases associated with injury of the heart muscle, including conditions without an obvious inflammatory pathogenic component such as hypertensive and diabetic cardiomyopathy. Persistence of cardiac inflammation can cause irreversible structural and functional deficits. Some are induced by direct damage of the heart muscle by cellular and soluble mediators but also by metabolic adaptations sustained by the inflammatory microenvironment. It is well established that both cardiomyocytes and immune cells undergo metabolic reprogramming in the site of inflammation, which allow them to deal with decreased availability of nutrients and oxygen. However, like in cancer, competition for nutrients and increased production of signalling metabolites such as lactate initiate a metabolic cross-talk between immune cells and cardiomyocytes which, we propose, might tip the balance between resolution of the inflammation versus adverse cardiac remodeling. Here we review our current understanding of the metabolic reprogramming of both heart tissue and immune cells during inflammation, and we discuss potential key mechanisms by which these metabolic responses intersect and influence each other and ultimately define the prognosis of the inflammatory process in the heart.
炎症过程是许多与心肌损伤相关疾病的基础，包括那些没有明显炎症致病成分的病症，如高血压性和糖尿病性心肌病。心脏炎症的持续存在会导致不可逆转的结构和功能缺陷。有些是由细胞和可溶性介质对心肌的直接损伤引起的，但也由炎症微环境维持的代谢适应引起。众所周知，心肌细胞和免疫细胞在炎症部位都会经历代谢重编程，这使它们能够应对营养物质和氧气供应减少的情况。然而，与癌症一样，对营养物质的竞争以及信号代谢物（如乳酸）产量的增加引发了免疫细胞与心肌细胞之间的代谢相互作用，我们认为，这可能会打破炎症消退与不良心脏重塑之间的平衡。在这里，我们回顾了目前对炎症期间心脏组织和免疫细胞代谢重编程的理解，并讨论了这些代谢反应相互交叉和相互影响的潜在关键机制，以及它们最终如何决定心脏炎症过程的预后。
