DeLeon-Pennell Kristine Y, Meschiari Cesar A, Jung Mira, Lindsey Merry L
Mississippi Center for Heart Research, UMMC, Jackson, MS, United States; Research Service, G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, MS, United States.
Mississippi Center for Heart Research, UMMC, Jackson, MS, United States.
Prog Mol Biol Transl Sci. 2017;147:75-100. doi: 10.1016/bs.pmbts.2017.02.001. Epub 2017 Mar 18.
Cardiovascular disease is the leading cause of death, accounting for 600,000 deaths each year in the United States. In addition, heart failure accounts for 37% of health care spending. Matrix metalloproteinases (MMPs) increase after myocardial infarction (MI) and correlate with left ventricular dysfunction in heart failure patients. MMPs regulate the remodeling process by facilitating extracellular matrix turnover and inflammatory signaling. Due to the critical role MMPs play during cardiac remodeling, there is a need to better understand the pathophysiological mechanism of MMPs, including the biological function of the downstream products of MMP proteolysis. Future studies developing new therapeutic targets that inhibit specific MMP actions to limit the development of heart failure post-MI are warranted. This chapter focuses on the role of MMPs post-MI, the efficiency of MMPs as biomarkers for MI or heart failure, and the future of MMPs and their cleavage products as targets for prevention of post-MI heart failure.
心血管疾病是主要的死亡原因，在美国每年导致60万人死亡。此外，心力衰竭占医疗保健支出的37%。心肌梗死后基质金属蛋白酶（MMPs）增加，并且与心力衰竭患者的左心室功能障碍相关。MMPs通过促进细胞外基质周转和炎症信号传导来调节重塑过程。由于MMPs在心脏重塑过程中发挥关键作用，因此有必要更好地了解MMPs的病理生理机制，包括MMP蛋白水解下游产物的生物学功能。开展未来研究以开发抑制特定MMP作用的新治疗靶点，从而限制心肌梗死后心力衰竭的发展是很有必要的。本章重点关注心肌梗死后MMPs的作用、MMPs作为心肌梗死或心力衰竭生物标志物的有效性，以及MMPs及其裂解产物作为预防心肌梗死后心力衰竭靶点的未来前景。
