Fernández-Solà Joaquim, Borrisser-Pairó Francesc, Antúnez Emilia, Tobías Ester
Alcohol Research Unit, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), CIBEROBN Fisiopatología de la Obesidad y la Nutrición, Instituto de Salud Carlos III (JF-S), Department of Medicine, University of Barcelona, Catalunya, Spain.
J Hypertens. 2015 Apr;33(4):851-8; discussion 859. doi: 10.1097/HJH.0000000000000493.
The physiopathological mechanisms implicated in hypertensive heart disease are multi-factorial, including myocyte hypertrophy, apoptosis and myocardial remodelling. In this process, some hormonal and local growth factors have a regulatory influence. The aim of this study was to evaluate the potential role of myostatin and insulin-like growth factor-1 (IGF-1) myocardial expression in the development of hypertensive-induced cardiac damage.
Samples of human myocardium tissue from organ donors were prospectively collected and classified according to the presence of hypertension, alcohol consumption, other causes of myocardial damage and the presence of structural cardiomyopathy (CMP). Myocardial samples were studied by immunohistochemistry and myostatin, and IGF-1 myocardial expression was evaluated in all the different groups of donors. Hypertensive donors were compared to other groups.
A total of 66 heart samples from human donors were collected: 33 donors had no previous or present history of hypertension and 33 donors presented defined hypertension. Donors with hypertension presented higher myocyte cell and nuclear hypertrophy and showed similar myostatin myocardial expression as controls, but lower IGF-1 myocardial expression. Myostatin expression was significantly higher in hypertensive donors with CMP compared to non-hypertensive healthy donors. The presence of CMP of diverse origin (alcoholic, valve and coronary) also significantly increased myostatin myocardial expression.
The presence of hypertension significantly decreases IGF-1 myocardial expression. Myostatin myocardial expression increases in the presence of structural CMP either of hypertensive or other origin. These effects open the possibility of modulating hypertensive-induced cardiac damage.
高血压性心脏病涉及的生理病理机制是多因素的，包括心肌细胞肥大、凋亡和心肌重塑。在此过程中，一些激素和局部生长因子具有调节作用。本研究的目的是评估肌肉生长抑制素和胰岛素样生长因子-1（IGF-1）心肌表达在高血压性心脏损伤发展中的潜在作用。
前瞻性收集器官捐献者的人类心肌组织样本，并根据是否存在高血压、饮酒情况、心肌损伤的其他原因以及是否存在结构性心肌病（CMP）进行分类。通过免疫组织化学研究心肌样本，评估所有不同组捐献者中肌肉生长抑制素和IGF-1的心肌表达。将高血压捐献者与其他组进行比较。
共收集了66例人类捐献者的心脏样本：33例捐献者既往或目前无高血压病史，33例捐献者患有明确的高血压。患有高血压的捐献者表现出更高的心肌细胞和细胞核肥大，其肌肉生长抑制素心肌表达与对照组相似，但IGF-1心肌表达较低。与非高血压健康捐献者相比，患有CMP的高血压捐献者的肌肉生长抑制素表达明显更高。不同来源（酒精性、瓣膜性和冠状动脉性）的CMP的存在也显著增加了肌肉生长抑制素的心肌表达。
高血压的存在显著降低IGF-1的心肌表达。无论是高血压性还是其他来源的结构性CMP存在时，肌肉生长抑制素的心肌表达都会增加。这些作用为调节高血压性心脏损伤提供了可能性。
