Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, MB R2H 2A6, Canada.
Department of Physiology and Pathophysiology, Rady Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, MB R3E 0J9, Canada.
Int J Mol Sci. 2024 Jan 16;25(2):1082. doi: 10.3390/ijms25021082.
With cardiovascular disease (CVD) being a primary source of global morbidity and mortality, it is crucial that we understand the molecular pathophysiological mechanisms at play. Recently, numerous pro-inflammatory cytokines have been linked to several different CVDs, which are now often considered an adversely pro-inflammatory state. These cytokines most notably include interleukin-6 (IL-6),tumor necrosis factor (TNF)α, and the interleukin-1 (IL-1) family, amongst others. Not only does inflammation have intricate and complex interactions with pathophysiological processes such as oxidative stress and calcium mishandling, but it also plays a role in the balance between tissue repair and destruction. In this regard, pre-clinical and clinical evidence has clearly demonstrated the involvement and dynamic nature of pro-inflammatory cytokines in many heart conditions; however, the clinical utility of the findings so far remains unclear. Whether these cytokines can serve as markers or risk predictors of disease states or act as potential therapeutic targets, further extensive research is needed to fully understand the complex network of interactions that these molecules encompass in the context of heart disease. This review will highlight the significant advances in our understanding of the contributions of pro-inflammatory cytokines in CVDs, including ischemic heart disease (atherosclerosis, thrombosis, acute myocardial infarction, and ischemia-reperfusion injury), cardiac remodeling (hypertension, cardiac hypertrophy, cardiac fibrosis, cardiac apoptosis, and heart failure), different cardiomyopathies as well as ventricular arrhythmias and atrial fibrillation. In addition, this article is focused on discussing the shortcomings in both pathological and therapeutic aspects of pro-inflammatory cytokines in CVD that still need to be addressed by future studies.
心血管疾病(CVD)是全球发病率和死亡率的主要原因,因此了解起作用的分子病理生理学机制至关重要。最近,许多促炎细胞因子与几种不同的 CVD 相关,这些因子现在通常被认为是一种不利的促炎状态。这些细胞因子中最著名的包括白细胞介素 6(IL-6)、肿瘤坏死因子(TNF)α 和白细胞介素 1(IL-1)家族等。炎症不仅与氧化应激和钙处理不当等病理生理过程有着错综复杂的相互作用,而且在组织修复和破坏之间的平衡中也起着作用。在这方面,临床前和临床证据清楚地表明,促炎细胞因子参与了许多心脏疾病,并具有动态特性;然而,到目前为止,这些发现的临床应用仍不清楚。这些细胞因子是否可以作为疾病状态的标志物或风险预测因子,或者作为潜在的治疗靶点,还需要进一步的广泛研究来充分了解这些分子在心脏病背景下所包含的复杂相互作用网络。本文将重点介绍我们对促炎细胞因子在 CVD 中的作用的理解的重要进展,包括缺血性心脏病(动脉粥样硬化、血栓形成、急性心肌梗死和缺血再灌注损伤)、心脏重构(高血压、心脏肥大、心脏纤维化、心脏细胞凋亡和心力衰竭)、不同的心肌病以及室性心律失常和心房颤动。此外,本文还重点讨论了 CVD 中促炎细胞因子在病理和治疗方面仍存在的不足之处,这些不足需要未来的研究来解决。