Department of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, TX, USA.
J Cardiovasc Pharmacol. 2012 Sep;60(3):248-52. doi: 10.1097/FJC.0b013e3182646cb1.
Stress-induced hypertrophic growth of the myocardium is a pathogenetic milestone in the progression of heart failure. Some evidence suggests that suppression of pathological cardiac hypertrophy per se is a viable target for therapeutic intervention, and cardiomyocyte autophagy is an attractive mechanism for consideration as a means of controlling the hypertrophic response. However, although considerable insights have been gleaned in the molecular mechanisms governing cardiomyocyte autophagy, many details critical to rational targeting of the response remain unknown. Among them, mechanisms underlying the adaptive and maladaptive features of autophagy are obscure. With time and further study, it is possible that this near-ubiquitous cardiac response to stress will emerge as a target for therapeutic manipulation.
应激诱导的心肌肥厚是心力衰竭进展中的一个病理里程碑。有证据表明，抑制病理性心肌肥厚本身就是一种可行的治疗干预靶点，而心肌细胞自噬是一种有吸引力的机制，可以作为控制肥厚反应的手段。然而，尽管在调控心肌细胞自噬的分子机制方面已经有了相当多的了解，但对于合理靶向反应的许多关键细节仍然未知。其中，自噬的适应性和失代偿性特征的机制尚不清楚。随着时间的推移和进一步的研究，这种对压力近乎普遍的心脏反应有可能成为治疗干预的靶点。
