Role of Heme Oxygenase-1 (HO-1) in the Pathogenesis of Hypertension among Young Adults: Association with Oxidative Stress, Inflammatory Markers, and Metabolic Profile
TL;DR
A distinct biochemical profile of young-adult hypertension is identified by reduced HO-1 and NO concentrations alongside increased VEGF, insulin, iron, and ADA concentrations, collectively reflecting metabolic dysregulation, impaired endothelial function, oxidative stress, and inflammatory activity.
Abstract
Hypertension in young adults is increasingly recognized as a multifactorial condition associated with oxidative stress, inflammation, endothelial dysfunction, and metabolic imbalance. This study investigated the relationship between heme oxygenase-1 (HO-1) and hypertension among young adults, with particular attention to oxidative stress markers, inflammatory mediators, and metabolic profiles. A case–control study was conducted involving 170 hypertensive and normotensive participants. Sociodemographic and clinical characteristics were assessed alongside blood pressure, body mass index (BMI), body weight, and biochemical markers, including HO-1, vascular endothelial growth factor (VEGF), insulin, nitric oxide (NO), iron, and adenosine deaminase (ADA). Compared with normotensive controls, hypertensive participants had significantly higher systolic and diastolic blood pressure (p < 0.05), as well as higher BMI and body weight. HO-1 concentrations were markedly lower in hypertensive participants (p < 0.00001), indicating reduced antioxidant capacity. Conversely, VEGF concentrations were significantly elevated (p < 0.00001), consistent with altered vascular regulation. Hypertensive participants also exhibited increased insulin concentrations (p < 0.01), reduced NO concentrations (p < 0.00001), and elevated iron and ADA concentrations (p < 0.00001), collectively reflecting metabolic dysregulation, impaired endothelial function, oxidative stress, and inflammatory activity. Correlation analysis revealed no significant associations between HO-1 and adenosine, ADA, or xanthine oxidase (p > 0.05). These findings identify a distinct biochemical profile of young-adult hypertension characterized by reduced HO-1 and NO concentrations alongside increased VEGF, insulin, iron, and ADA concentrations. Although the case–control design does not establish causality, the results highlight HO-1 as a relevant component of the oxidative and vascular alterations associated with hypertension and support further longitudinal and mechanistic investigation.