Department of Medicine, Vermont Center for Immunology and Infectious Diseases, University of Vermont, Burlington, VT, 05405, USA.
J Cardiovasc Transl Res. 2014 Mar;7(2):182-91. doi: 10.1007/s12265-013-9525-5. Epub 2013 Dec 10.
Under normal conditions, autophagy maintains cardiomyocyte health and integrity through turnover of organelles. During stress, oxygen and nutrient deprivation, or microbial infection, autophagy prolongs cardiomyocyte survival. Sex differences in induction of cell death may to some extent explain the disparity between the sexes in many human diseases. However, sex differences in gene expression, which regulate cell death and autophagy, were so far not taken in consideration to explain the sex bias of viral myocarditis. Coxsackievirus B3 (CVB3)-induced myocarditis is a sex-biased disease, with females being substantially less susceptible than males and sex hormones largely determine this bias. CVB3 was shown to induce and subvert the autophagosome for its optimal viral RNA replication. Gene expression analysis on mouse and human, healthy and CVB3-infected, cardiac samples of both sexes, suggests sex differences in autophagy-related gene expression. This review discusses the aspects of sex bias in autophagy induction in cardiomyocytes.
在正常条件下，自噬通过细胞器的更新来维持心肌细胞的健康和完整。在应激、缺氧和营养剥夺或微生物感染时，自噬会延长心肌细胞的存活时间。细胞死亡诱导的性别差异在一定程度上可以解释许多人类疾病中性别差异的现象。然而，调节细胞死亡和自噬的基因表达的性别差异迄今尚未被考虑用来解释病毒性心肌炎的性别偏向。柯萨奇病毒 B3（CVB3）诱导的心肌炎是一种性别偏向性疾病，女性的易感性明显低于男性，而性激素在很大程度上决定了这种偏向。CVB3 已被证明可以诱导和颠覆自噬体以实现最佳的病毒 RNA 复制。对来自不同性别、健康和 CVB3 感染的小鼠和人类心脏样本的基因表达分析表明，自噬相关基因表达存在性别差异。本文讨论了诱导心肌细胞自噬中的性别偏向性的相关方面。
