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Emerging evidence highlights the critical role of mitochondrial dysfunction in HCH pathogenesis, with impaired mitophagy\u2014a selective autophagic process that removes damaged mitochondria\u2014contributing to cardiomyocyte death, oxidative stress, and fibrosis. Protective mitophagy eliminates damaged mitochondria, averting reactive oxygen species (ROS)\/calcium overload in HCH. Conversely, its dysregulation\u2014either insufficient clearance or excessive removal\u2014exacerbates mitochondrial dysfunction, driving pathological hypertrophy, fibrosis, and bioenergetic crisis. This dual nature presents a therapeutic paradox demanding contextual modulation. This review comprehensively examines the molecular mechanisms underlying mitophagy dysregulation in HCH, focusing on key pathways such as PINK1\/Parkin, BNIP3\/NIX, and FUNDC1. We also discuss the interplay between mitophagy and other cellular processes, including mitochondrial biogenesis, inflammasome activation, and metabolic remodeling. Furthermore, we explore potential therapeutic strategies targeting mitophagy to ameliorate HCH, including pharmacological agents, lifestyle interventions, and gene therapy approaches. Understanding the dual role of mitophagy in HCH\u2014both protective and detrimental\u2014may pave the way for novel precision medicine strategies in cardiovascular disease.<\/jats:p>","DOI":"10.1111\/jch.70127","type":"journal-article","created":{"date-parts":[[2025,8,18]],"date-time":"2025-08-18T10:46:52Z","timestamp":1755514012000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Mitophagy in Hypertensive Cardiac Hypertrophy: Mechanisms and Therapeutic Implications"],"prefix":"10.1111","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-6496-287X","authenticated-orcid":false,"given":"Shijun","family":"Li","sequence":"first","affiliation":[{"name":"Department of Hainan Health Care The Second Medical Center of Chinese PLA General Hospital at Haitang Bay  Sanya Hainan PR 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