Pahlavani Hamed Alizadeh
Department of Physical Education, Farhangian University, Tehran, Iran.
Front Cell Dev Biol. 2022 Aug 11;10:950927. doi: 10.3389/fcell.2022.950927. eCollection 2022.
Cardiovascular diseases are the most common cause of death in the world. One of the major causes of cardiac death is excessive apoptosis. However, multiple pathways through moderate exercise can reduce myocardial apoptosis. After moderate exercise, the expression of anti-apoptotic proteins such as IGF-1, IGF-1R, p-PI3K, p-Akt, ERK-1/2, SIRT3, PGC-1α, and Bcl-2 increases in the heart. While apoptotic proteins such as PTEN, PHLPP-1, GSK-3, JNK, P38MAPK, and FOXO are reduced in the heart. Exercise-induced mechanical stress activates the β and α5 integrins and subsequently, focal adhesion kinase phosphorylation activates the Akt/mTORC1 and ERK-1/2 pathways, leading to an anti-apoptotic response. One of the reasons for the decrease in exercise-induced apoptosis is the decrease in Fas-ligand protein, Fas-death receptor, TNF-α receptor, Fas-associated death domain (FADD), caspase-8, and caspase-3. In addition, after exercise mitochondrial-dependent apoptotic factors such as Bid, t-Bid, Bad, p-Bad, Bak, cytochrome c, and caspase-9 are reduced. These changes lead to a reduction in oxidative damage, a reduction in infarct size, a reduction in cardiac apoptosis, and an increase in myocardial function. After exercising in the heart, the levels of RhoA, ROCK1, Rac1, and ROCK2 decrease, while the levels of PKCε, PKCδ, and PKCɑ are activated to regulate calcium and prevent mPTP perforation. Exercise has an anti-apoptotic effect on heart failure by increasing the PKA-Akt-eNOS and FSTL1-USP10-Notch1 pathways, reducing the negative effects of CaMKIIδ, and increasing the calcineurin/NFAT pathway. Exercise plays a protective role in the heart by increasing HSP20, HSP27, HSP40, HSP70, HSP72, and HSP90 along with increasing JAK2 and STAT3 phosphorylation. However, research on exercise and factors such as Pim-1, Notch, and FAK in cardiac apoptosis is scarce, so further research is needed. Future research is recommended to discover more anti-apoptotic pathways. It is also recommended to study the synergistic effect of exercise with gene therapy, dietary supplements, and cell therapy for future research.
心血管疾病是全球最常见的死亡原因。心脏死亡的主要原因之一是过度凋亡。然而,适度运动可通过多种途径减少心肌凋亡。适度运动后,心脏中抗凋亡蛋白如IGF-1、IGF-1R、p-PI3K、p-Akt、ERK-1/2、SIRT3、PGC-1α和Bcl-2的表达增加。而凋亡蛋白如PTEN、PHLPP-1、GSK-3、JNK、P38MAPK和FOXO在心脏中减少。运动诱导的机械应力激活β和α5整合素,随后,粘着斑激酶磷酸化激活Akt/mTORC1和ERK-1/2途径,导致抗凋亡反应。运动诱导的凋亡减少的原因之一是Fas配体蛋白、Fas死亡受体、TNF-α受体、Fas相关死亡结构域(FADD)、半胱天冬酶-8和半胱天冬酶-3的减少。此外,运动后线粒体依赖性凋亡因子如Bid、t-Bid、Bad、p-Bad、Bak、细胞色素c和半胱天冬酶-9减少。这些变化导致氧化损伤减少、梗死面积减小、心脏凋亡减少以及心肌功能增强。心脏运动后,RhoA、ROCK1、Rac1和ROCK2水平降低,而PKCε、PKCδ和PKCɑ水平被激活以调节钙并防止线粒体通透性转换孔(mPTP)穿孔。运动通过增加PKA-Akt-eNOS和FSTL1-USP10-Notch1途径、减少CaMKIIδ的负面影响以及增加钙调神经磷酸酶/NFAT途径,对心力衰竭具有抗凋亡作用。运动通过增加HSP20、HSP27、HSP40、HSP70、HSP72和HSP90以及增加JAK2和STAT3磷酸化,对心脏起到保护作用。然而,关于运动与心脏凋亡中的Pim-1、Notch和FAK等因素的研究较少,因此需要进一步研究。建议未来的研究发现更多的抗凋亡途径。还建议研究运动与基因治疗、膳食补充剂和细胞治疗的协同作用以供未来研究。