Faculty Unit of Anatomy and Morphology, University Centre of Legal Medicine, Lausanne-Geneva, Rue du Bugnon 9, 1005 Lausanne, Switzerland.
Faculty Unit of Anatomy and Morphology, University Centre of Legal Medicine, Lausanne-Geneva, Rue du Bugnon 9, 1005 Lausanne, Switzerland; Unit of Forensic medicine, University Centre of Legal Medicine, Lausanne-Geneva, Rue Michel-Servet 1, 1211 Geneva, Switzerland.
Cardiovasc Pathol. 2025 Jan-Feb;74:107691. doi: 10.1016/j.carpath.2024.107691. Epub 2024 Aug 31.
Myocardial infarction (MI) is a life-threatening condition that leads to loss of viable heart tissue. The best way to treat acute MI and limit the infarct size is to re-open the occluded coronary artery and restore the supply of oxygenated and nutrient-rich blood, but reperfusion can cause additional damage. Autophagy is an intracellular process that recycles damaged cytoplasmic components (molecules and organelles) by loading them into autophagosomes and degrading them in autolysosomes. Autophagy is increased in in vivo animal models of permanent ischemia and ischemia/reperfusion but by different molecular mechanisms. While autophagy is protective during permanent ischemia, it is detrimental during ischemia/reperfusion. Its modulation is being investigated as a potential target to reduce reperfusion injury. This review provides a synopsis of the current knowledge about autophagy, summarizes findings specifically in permanent ischemia and ischemia/reperfusion, and briefly discusses the potential implication of experimental findings.
心肌梗死（MI）是一种危及生命的疾病，可导致心肌组织坏死。治疗急性 MI 并限制梗死面积的最佳方法是重新开放闭塞的冠状动脉并恢复含氧和富含营养的血液供应，但再灌注可能会导致额外的损伤。自噬是一种通过将受损的细胞质成分（分子和细胞器）装入自噬体并在自溶酶体中降解来回收它们的细胞内过程。在永久性缺血和缺血/再灌注的动物模型中，自噬增加，但分子机制不同。虽然自噬在永久性缺血期间具有保护作用，但在缺血/再灌注期间却有害。目前正在研究其调节作为减少再灌注损伤的潜在靶点。本文综述了自噬的最新知识，总结了永久性缺血和缺血/再灌注中特定的发现，并简要讨论了实验发现的潜在意义。
