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MCJ levels elevate under hypoxic conditions, as in lungs of patients affected by COPD, mice exposed to hypoxia, and myocardium from pigs subjected to right ventricular (RV) overload. The absence of MCJ preserves RV function, safeguarding against both cardiac and lung remodeling induced by chronic hypoxia. Cardiac-specific silencing is enough to protect against cardiac dysfunction despite the adverse pulmonary remodeling. Mechanistically, the absence of MCJ triggers a protective preconditioning state mediated by the ROS\/mTOR\/HIF-1\u03b1 axis. As a result, it preserves RV systolic function following hypoxia exposure. These discoveries provide a potential avenue to alleviate chronic hypoxia-induced PH, highlighting MCJ as a promising target against this condition.<\/jats:p>","DOI":"10.1126\/sciadv.adk6524","type":"journal-article","created":{"date-parts":[[2024,1,19]],"date-time":"2024-01-19T18:58:32Z","timestamp":1705690712000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":9,"title":["MCJ: A mitochondrial target for cardiac intervention in pulmonary hypertension"],"prefix":"10.1126","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9487-7238","authenticated-orcid":true,"given":"Ayel\u00e9n M.","family":"Santamans","sequence":"first","affiliation":[{"name":"Cardiovascular Risk Factors and Brain Function Program, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, 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