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Moreover, they can achieve the purpose of protecting cells by maintaining mitochondrial function and dynamics [mitochondrial dysfunction can contribute to the development of inflammatory lung diseases (Kellner et al., 2017)]

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It can improve the imbalance of cardiac mitochondrial dynamics, excessive mitophagy, and mitochondrial dysfunction caused by aging, reduce the protein levels of Bax and cleaved-caspase-3, increase the expression of Bcl-2 protein, inhibit myocardial cell apoptosis, and improve mitochondrial and cardiac function in aging rats ( 5.2.3 Exercise regulates mitophagy to inhibit inflammatory response Inflammatory responses are closely associated with the development of metabolic diseases ( 5.2.4 Exercise-mediated exerkines regulate mitophagy Exercise stimulates the release of specific endogenous cytokines, peptides, nucleic acids, and metabolites from skeletal muscle and other endocrine organs, collectively called exerkines, which have a crucial regulatory role in maintaining cellular functional homeostasis and quality control ( 40 and A 42 levels, and improved learning and memory ability in APP/PS1 transgenic mice, suggesting that the SIRT1-FOXO1/3 signaling pathway is a potential target for exercise-enhanced mitophagy ( 6 Conclusion and perspectives Mitophagy is an essential regulatory mechanism that ensures the homeostasis of mitochondrial number and mass and maintains cell survival

[195] found that administration of HRS suppresses the expression of proinflammatory cytokines IL1 and TNF, as well as inhibits the activation of NFB in intestinal I/R mice, thereby attenuating the damage caused by intestinal I/R (Figure 4)