bims-mitrat 2025-04-13 papers

Elife. 2025 Apr 10. pii: RP98554. [Epub ahead of print]13

Transplantation of exogenous mitochondria mitigates myocardial dysfunction after cardiac arrest.

Zhen Wang, Jie Zhu, Mengda Xu, Xuyuan Ma, Maozheng Shen, Jingyu Yan, Guosheng Gan, Xiang Zhou.

The incidence of post-cardiac arrest myocardial dysfunction (PAMD) is high, and there is currently no effective treatment available. This study aims to investigate the protective effects of exogenous mitochondrial transplantation in Sprague-Dawley (SD) rats. Exogenous mitochondrial transplantation can enhance myocardial function and improve the survival rate. Mechanistic studies suggest that mitochondrial transplantation can limit impairment in mitochondrial morphology, augment the activity of mitochondrial complexes II and IV, and raise ATP level. As well, mitochondrial therapy ameliorated oxidative stress imbalance, reduced myocardial injury, and thus improved PAMD after cardiopulmonary resuscitation (CPR).

Keywords: apoptosis; medicine; mitochondria; muscle fiber; rat

DOI: https://doi.org/10.7554/eLife.98554

Mol Cell. 2025 Apr 03. pii: S1097-2765(25)00188-1. [Epub ahead of print]85(7): 1258-1259

Hijacking the powerhouse: Mitochondrial transfer and mitophagy as emerging mechanisms of immune evasion.

Maria T Diaz-Meco, Juan F Linares, Jorge Moscat.

Cancer cells subvert the immune system by reprogramming their metabolism. In a recent study in Nature, Ikeda et al.1 show how cancer cells can directly transfer mitophagy-resistant mitochondria to tumor-infiltrating lymphocytes, promoting their homoplasmic replacement and undermining cancer immunity.

DOI: https://doi.org/10.1016/j.molcel.2025.02.026

J Transl Med. 2025 Apr 10. 23(1): 418

Mitochondrial dysfunction in AMI: mechanisms and therapeutic perspectives.

Jingle Shi, Yiding Yu, Huajing Yuan, Yan Li, Yitao Xue.

Acute myocardial infarction (AMI) and the myocardial ischemia-reperfusion injury (MI/RI) that typically ensues represent a significant global health burden, accounting for a considerable number of deaths and disabilities. In the context of AMI, percutaneous coronary intervention (PCI) is the preferred treatment option for reducing acute ischemic damage to the heart. Despite the modernity of PCI therapy, pathological damage to cardiomyocytes due to MI/RI remains an important target for intervention that affects the long-term prognosis of patients. In recent years, mitochondrial dysfunction during AMI has been increasingly recognized as a critical factor in cardiomyocyte death. Damaged mitochondria play an active role in the formation of an inflammatory environment by triggering key signaling pathways, including those mediated by cyclic GMP-AMP synthase, NOD-like receptors and Toll-like receptors. This review emphasizes the dual role of mitochondria as both contributors to and regulators of inflammation. The aim is to explore the complex mechanisms of mitochondrial dysfunction in AMI and its profound impact on immune dysregulation. Specific interventions including mitochondrial-targeted antioxidants, membrane-stabilizing peptides, and mitochondrial transplantation therapies have demonstrated efficacy in preclinical AMI models.

Keywords: Acute myocardial infarction; Cell death; Inflammatory response; Mitochondrial damage; Myocardial ischemia-reperfusion injury; Therapeutic strategy

DOI: https://doi.org/10.1186/s12967-025-06406-5