Reviewing the suitability of mitochondrial transplantation as therapeutic approach for pulmonary hypertension in the era of personalized medicine

Pulmonary hypertension (PH) is a fatal disease, defined as a mean pulmonary artery pressure ≥25 mmHg. It is caused, in part, by mitochondrial dysfunction. Among the various biological therapies proposed to rescue mitochondrial dysfunction, evidence going back as far as 2009 suggests that mitochondrial transplantation is an alternative. Although scant, recent PH findings and other literature support a role for mitochondrial transplantation as a therapeutic approach in the context of PH. In experimental models of PH, it confers beneficial effects that include reduced pulmonary vasoconstriction, reduced pulmonary vascular remodeling, and improved right ventricular function. It also reduces the proliferation of pulmonary artery smooth muscle cells. However, first, we must understand that more research is needed before mitochondrial transplantation can be considered an effective therapy in the clinical setting, as many of the mechanisms or potential long-term risks are still unknown. Second, the current challenges of mitochondrial transplantation are surmountable and should not deter researchers from further investigating its effectiveness and trying to overcome these challenges in creative ways.