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Mitochondria play a pivotal role in energy generation and cellular physiological processes. These organelles are highly dynamic, constantly changing their morphology, cellular location, and distribution in response to cellular stress. In recent years, the phenomenon of mitochondrial transfer has attracted significant attention and interest from biologists and medical investigators. Intercellular mitochondrial transfer occurs in different ways, including tunnelling nanotubes (TNTs), extracellular vesicles (EVs), and gap junction channels (GJCs). According to research on intercellular mitochondrial transfer in physiological and pathological environments, mitochondrial transfer hold great potential for maintaining body homeostasis and regulating pathological processes. Multiple research groups have developed artificial mitochondrial transfer/transplantation (AMT/T) methods that transfer healthy mitochondria into damaged cells and recover cellular function. This paper reviews intercellular spontaneous mitochondrial transfer modes, mechanisms, and the latest methods of AMT/T. Furthermore, potential application value and mechanism of AMT/T in disease treatment are also discussed.

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A polarized macrophage response plays a critical role in the pathophysiological process of myocardial infarction (MI). Several studies have shown a pro-inflammatory role for monomeric C-reactive protein (mCRP) in cardiovascular disease. However, the mechanism of how mCRP regulates macrophage phenotype switching remains unknown. In the present study, the effect of mCRP on macrophage polarization and its pathological function in myocardial repair after myocardial infarction was investigated. Methods: MI was induced by permanent ligation of the left anterior descending coronary artery in ICR mice. Adult mice were injected with mCRP (2.5 mg/kg) with or without SP600125 (15 mg/kg, JNK inhibitor) 45 min before MI. The cardiac function, scar size as well as cardiac fibrosis, infiltration of inflammatory cells, and the level of proteins in the JNK signaling pathway in infarcted myocardium were assessed. In addition, the phenotypic characterization of macrophages was further measured by ELISA, flow cytometry and quantitative RT-PCR in cultured THP-1 cells or peritoneal macrophages. Results: Cardiac function deterioration, ventricular dilatation and fibrosis were exacerbated in mice pretreatment with mCRP following MI. Meanwhile, an increased accumulation of infiltrated inflammatory cells in infarcted myocardium was observed in the mCRP group. Moreover, activation of the JNK signaling pathway was markedly elevated in mCRP treated animals post-MI. In contrast, pharmacological inhibition of JNK phosphorylation activity by SP600125 muted the detrimental effects of mCRP in MI mice. Furthermore, in vitro and in vivo co-culture experiments showed that mCRP shifted macrophage polarization towards pro-inflammatory phenotypes, and this polarization could be abolished by sp600125. Conclusion: Taken together, our results imply that mCRP impairs myocardial repair after myocardial infarction by polarizing the macrophages into the pro-inflammatory M1 phenotype via the JNK-dependent pathway.

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