Recent advances in the pathophysiology of hypertension highlight the roles of oxidative stress, mitochondrial dysfunction, inflammation, epigenetics, non-coding RNAs, and alamandine.
This review summarizes recent advances in understanding the complex molecular and pathophysiological mechanisms underlying hypertension.
High blood pressure (hypertension) is a complex, multifactorial and multisystem disorder and a leading cause of morbidity and premature death worldwide. It is the major modifiable risk factor for heart disease, stroke and kidney disease. The underlying cause of hypertension is identified in ∼5% of patients (secondary hypertension), while in 95% of patients, no specific etiology is found (primary hypertension). Multiple factors including genetics, environmental elements, hemodynamics and interacting physiological systems contribute to the pathophysiology of hypertension. At the molecular level, growing evidence indicates an important role for oxidative stress, mitochondrial dysfunction, inflammation, epigenetics and non-coding RNAs. In addition, new components of the renin angiotensin system, including alamandine, have been discovered as potential players in the development of hypertension. Here we highlight some novel concepts on molecular mechanisms and pathophysiological processes underlying hypertension.
Montezano et al. (Tue,) conducted a review in Hypertension. Recent advances in the pathophysiology of hypertension highlight the roles of oxidative stress, mitochondrial dysfunction, inflammation, epigenetics, non-coding RNAs, and alamandine.