Center of Basic Research, Biomedical Research Foundation of the Academy of Athens, Soranou Efesiou 4, 115 27 Athens, Greece.
Biomolecules. 2024 Nov 4;14(11):1403. doi: 10.3390/biom14111403.
Stromal and immune cells and their interactions have gained the attention of cardiology researchers and clinicians in recent years as their contribution in cardiac repair is increasingly recognized. The repair process in the heart is a particularly critical constellation of complex molecular and cellular events and interactions that characteristically fail to ensure adequate recovery following injury, insult, or exposure to stress conditions in this regeneration-hostile organ. The tremendous consequence of this pronounced inability to maintain homeostatic states is being translated in numerous ways promoting progress into heart failure, a deadly, irreversible condition requiring organ transplantation. Fibrosis is in fact a repair response eventually promoting cardiac dysfunction and cardiac fibroblasts are the major cellular players in this process, overproducing collagens and other extracellular matrix components when activated. On the other hand, macrophages may differentially affect fibroblasts and cardiac repair depending on their status and subsets. The opposite interaction is also probable. We discuss here the multifaceted aspects and crosstalk of this cell dipole and the opportunities it may offer for beneficial manipulation approaches that will hopefully lead to progress in heart disease interventions.
近年来，基质和免疫细胞及其相互作用引起了心脏病学研究人员和临床医生的关注，因为人们越来越认识到它们在心脏修复中的作用。心脏的修复过程是一组特别复杂的分子和细胞事件及相互作用，其特征是在受伤、损伤或暴露于这种再生不利的器官的应激条件后，不能确保充分的恢复。这种明显缺乏维持体内平衡状态的巨大后果，正在以多种方式转化，促进心力衰竭的进展，心力衰竭是一种致命的、不可逆转的疾病，需要进行器官移植。纤维化实际上是一种修复反应，最终导致心脏功能障碍，而心脏成纤维细胞是这个过程中的主要细胞参与者，在被激活时会过度产生胶原蛋白和其他细胞外基质成分。另一方面，巨噬细胞根据其状态和亚群的不同，可能会对成纤维细胞和心脏修复产生不同的影响。相反的相互作用也是可能的。我们在这里讨论这个细胞偶极子的多方面方面和串扰，以及它可能为有益的操纵方法提供的机会，希望这将导致心脏病干预方面的进展。
