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.

/pdf/exercise-induced-signaling-pathways-to-counteracting-cardiac-q6yl8tsx.pdf

Exercise-induced signaling pathways to counteracting cardiac apoptotic processes

Involvement of mitochondrial dynamics and mitophagy in diabetic endothelial dysfunction and cardiac microvascular injury.

Impact of Geroscience on Therapeutic Strategies for Older Adults With Cardiovascular Disease: JACC Scientific Statement.

Abstract Background Mesenchymal Stromal Cells (MSC) have been widely used for their therapeutic properties in many clinical applications including myocardial infarction. Despite promising preclinical results and evidences of safety and efficacy in phases I/ II, inconsistencies in phase III trials have been reported. In a previous study, we have shown using MSC derived from the bone marrow of PPARβ/δ (Peroxisome proliferator-activated receptors β/δ) knockout mice that the acute cardioprotective properties of MSC during the first hour of reperfusion are PPARβ/δ-dependent but not related to the anti-inflammatory effect of MSC. However, the role of the modulation of PPARβ/δ expression on MSC cardioprotective and anti-apoptotic properties has never been investigated. Objectives The aim of this study was to investigate the role of PPARβ/δ modulation (inhibition or activation) in MSC therapeutic properties in vitro and ex vivo in an experimental model of myocardial infarction. Methods and results Naïve MSC and MSC pharmacologically activated or inhibited for PPARβ/δ were challenged with H 2 O 2 . Through specific DNA fragmentation quantification and qRT-PCR experiments, we evidenced in vitro an increased resistance to oxidative stress in MSC pre-treated by the PPARβ/δ agonist GW0742 versus naïve MSC. In addition, PPARβ/δ-priming allowed to reveal the anti-apoptotic effect of MSC on cardiomyocytes and endothelial cells in vitro. When injected during reperfusion, in an ex vivo heart model of myocardial infarction, 3.75 × 10 5 PPARβ/δ-primed MSC/heart provided the same cardioprotective efficiency than 7.5 × 10 5 naïve MSC, identified as the optimal dose in our experimental model. This enhanced short-term cardioprotective effect was associated with an increase in both anti-apoptotic effects and the number of MSC detected in the left ventricular wall at 1 h of reperfusion. By contrast, PPARβ/δ inhibition in MSC before their administration in post-ischemic hearts during reperfusion decreased their cardioprotective effects. Conclusion Altogether these results revealed that PPARβ/δ-primed MSC exhibit an increased resistance to oxidative stress and enhanced anti-apoptotic properties on cardiac cells in vitro . PPARβ/δ-priming appears as an innovative strategy to enhance the cardioprotective effects of MSC and to decrease the therapeutic injected doses. These results could be of major interest to improve MSC efficacy for the cardioprotection of injured myocardium in AMI patients. 

/pdf/pparb-d-priming-enhances-the-anti-apoptotic-and-therapeutic-27smq91k.pdf

PPARβ/δ priming enhances the anti-apoptotic and therapeutic properties of mesenchymal stromal cells in myocardial ischemia–reperfusion injury

Exercise may ameliorate the eventual heart failure inherent in human aging. In this study, we use zebrafish to understand how aging and exercise affect cardiomyocyte turnover and myocardial remodelling. We show that cardiomyocyte proliferation remains constant throughout life but that onset of fibrosis is associated with a late increase in apoptosis. These findings correlate with decreases in voluntary swimming activity, critical swimming speed (Ucrit), and increases in biomarkers of cardiac insufficiency. The ability to respond to severe physiological stress is also impaired with age. Although young adult fish respond with robust cardiomyocyte proliferation in response to enforced swimming, this is dramatically impaired in older fish and served by a smaller proliferation-competent cardiomyocyte population. Finally, we show that these aging responses can be improved through increased activity throughout adulthood. However, despite improvement in Ucrit and the proliferative response to stress, the size of the proliferating cardiomyocyte population remained unchanged. The zebrafish heart models human aging and reveals the important trade-off between preserving cardiovascular fitness through exercise at the expense of accelerated fibrotic change.

/pdf/exercise-programmed-cell-death-and-exhaustion-of-4ddhf4crld.pdf

Exercise, programmed cell death and exhaustion of cardiomyocyte proliferation in aging zebrafish.

The leading cause of heart failure is cardiomyopathy and damage to the cardiomyocytes. Adult mammalian cardiomyocytes have the ability to regenerate, but this cannot wholly compensate for myocardial cell loss after myocardial injury. Studies have shown that exercise has a regulatory role in the activation and promotion of regeneration of healthy and injured adult cardiomyocytes. However, current research on the effects of aerobic exercise in myocardial regeneration is not comprehensive. This review discusses the relationships between aerobic exercise and the regeneration of cardiomyocytes with respect to complex molecular and cellular mechanisms, paracrine factors, transcriptional factors, signaling pathways, and microRNAs that induce cardiac regeneration. The topics discussed herein provide a knowledge base for physical activity-induced cardiomyocyte regeneration, in which exercise enhances overall heart function and improves the efficacy of cardiac rehabilitation.

https://www.mdpi.com/2218-273X/11/1/19/pdf

The Molecular Mechanisms Associated with Aerobic Exercise-Induced Cardiac Regeneration.

Intrauterine environment during pregnancy has important effects on the cardiovascular development of the offspring, which could persist into adulthood. However, it is largely unknown whether maternal exercise during pregnancy has a beneficial effect on cardiac structure and function in the offspring of spontaneously hypertensive rats (SHR). PURPOSE: To investigate the effects of prenatal exercise on cardiac morphology and function in 3-month-old male offspring of SHR. METHODS: Pregnant SHR and Wistar-Kyoto rats (WKY) were separated into a sedentary group (p-WKY-SED, p-SHR-SED) and an exercise group (p-WKY-EX, p-SHR-EX) at random. Exercise group were subjected to swimming (60 min/day, 6 day/week, gestation day 1-19). Physical characteristics, myocardial cell morphology, myocardial collagen volume fraction (CVF%) and cardiac function of male offspring were evaluated at 3 months (3 M). RESULTS: 1) Prenatal exercise significantly decreased the diastolic blood pressure (DBP) and mean arterial pressure (MAP) in the offspring of SHR (DBP: 153.5 ± 2.12 vs. 146.7 ± 1.38 mmHg, p < 0.01; MAP: 169.3 ± 2.60 vs. 161.9 ± 3.82 mmHg, p < 0.01). 2) Prenatal exercise significantly decreased the left ventricular hypertrophy index at 3 M in the offspring of SHR (0.74 ± 0.01 vs. 0.70 ± 0.02, p < 0.05). 3) Loosely arranged cardiomyocytes and significant increase in CVF% in the pathological state of hypertension (6.13 ± 0.70 vs. 20.33 ± 1.36 p < 0.01). Prenatal exercise improved cardiomyocyte morphology and decreased CVF% in the offspring of SHR (20.33 ± 1.36 vs. 14.91 ± 0.72 p < 0.05). 4) Echocardiographic results showed that the p-SHR-SED group had a lower left ventricular ejection fraction (LVEF%) (82.33 ± 4.14 vs. 74.14 ± 1.92 p < 0.05), lower cardiac output (CO) (137 ± 6 vs. 100 ± 5 ml/min, p < 0.05) and significantly lower left ventricular short-axis contraction rate (LVFS%) (52.93 ± 1.56 vs. 42.81 ± 1.05, p < 0.01) compared to the p-WKY-SED group, while the exercise group showed no significant differences compared to their respective sedentary control groups (p > 0.05). CONCLUSION: Prenatal exercise significantly reduces DBP and MAP in 3 M male offspring of SHR and improves cardiac morphology in the pathological state, but do not significantly improve cardiac function.Supported by the National Natural Science Foundation of China 32071174. 

Effects Of Prenatal Exercise On Cardiac Morphology And Function In SHR Offspring

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The Molecular Mechanisms Associated with Aerobic Exercise-Induced Cardiac Regeneration.

Effects Of Prenatal Exercise On Cardiac Morphology And Function In SHR Offspring