Alfonso Eirin1, Amir Lerman2, Lilach O Lerman3,4. 1. Division of Nephrology and Hypertension, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA. 2. Department of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA. 3. Division of Nephrology and Hypertension, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA. Lerman.Lilach@Mayo.Edu. 4. Department of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA. Lerman.Lilach@Mayo.Edu.
Abstract
PURPOSE OF REVIEW: This review summarizes literature pertaining to the dawning field of therapeutic targeting of mitochondria in hypertension and discusses the potential of these interventions to ameliorate hypertension-induced organ damage. RECENT FINDINGS: In recent years, mitochondrial dysfunction has been reported as an important contributor to the pathogenesis of hypertension-related renal, cardiac, and vascular disease. This in turn prompted development of novel mitochondria-targeted compounds, some of which have shown promising efficacy in experimental studies and safety in clinical trials. In addition, drugs that do not directly target mitochondria have shown remarkable benefits in preserving these organelles in experimental hypertension. Enhancing mitochondrial health is emerging as a novel feasible approach to treat hypertension. Future perspectives include mechanistic experimental studies to establish a cause-effect relationship between mitochondrial dysfunction and hypertension and further clinical trials to confirm the reno-, cardio-, and vasculo-protective properties of these compounds in hypertension.
PURPOSE OF REVIEW: This review summarizes literature pertaining to the dawning field of therapeutic targeting of mitochondria in hypertension and discusses the potential of these interventions to ameliorate hypertension-induced organ damage. RECENT FINDINGS: In recent years, mitochondrial dysfunction has been reported as an important contributor to the pathogenesis of hypertension-related renal, cardiac, and vascular disease. This in turn prompted development of novel mitochondria-targeted compounds, some of which have shown promising efficacy in experimental studies and safety in clinical trials. In addition, drugs that do not directly target mitochondria have shown remarkable benefits in preserving these organelles in experimental hypertension. Enhancing mitochondrial health is emerging as a novel feasible approach to treat hypertension. Future perspectives include mechanistic experimental studies to establish a cause-effect relationship between mitochondrial dysfunction and hypertension and further clinical trials to confirm the reno-, cardio-, and vasculo-protective properties of these compounds in hypertension.
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