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Hyperhomocysteinemia-induced Nrf2/HO-1 pathway suppression aggravates cardiac remodeling of hypertensive rats

Ping Cao1, Wangmeng Zhang2, Xue Kong3

  • 1Department of Cardiology, Shandong Provincial Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China; Department of Geriatrics, Tai'an City Central Hospital, Taian, Shandong, China.

Biochemical and Biophysical Research Communications
|February 20, 2021
PubMed

Insights

Hypertension and hyperhomocysteinemia (HHcy) worsen cardiac remodeling by increasing oxidative stress and inhibiting the Nrf2/HO-1 pathway. This effect is more pronounced in hypertensive rats, highlighting a key mechanism in heart disease progression.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Pathophysiology of Hypertensive Heart Disease

Background:

  • Hypertension and hyperhomocysteinemia (HHcy) are known contributors to cardiac remodeling in hypertensive heart disease.
  • The precise mechanisms underlying collagen accumulation and cardiac remodeling in this context remain incompletely understood.

Purpose of the Study:

  • To investigate the relationship between hypertension and HHcy in relation to cardiac remodeling.
  • To elucidate the underlying molecular mechanisms driving cardiac remodeling in the presence of HHcy and hypertension.

Main Methods:

  • Wistar Kyoto (WKY) and spontaneous hypertension rats (SHR) were subjected to four experimental groups: control, HHcy, hypertension, and combined HHcy and hypertension.
  • Key physiological and biochemical markers were measured, including blood pressure, plasma homocysteine (Hcy), serum superoxide dismutase (SOD), and serum malondialdehyde (MDA).
  • Cardiac histopathology was assessed, alongside the gene and protein expression of Nrf2 and HO-1, and Nrf2 translocation.

Main Results:

  • Progressive increases in myocardial collagen deposition and cardiac remodeling were observed across groups, with HHcy exacerbating remodeling more severely in hypertensive rats.
  • Serum SOD levels decreased, while MDA levels increased, indicating elevated oxidative stress.
  • Both HHcy and hypertension suppressed Nrf2 and HO-1 expression and inhibited Nrf2 nuclear translocation, with a more pronounced effect in the combined hypertension and HHcy group.

Conclusions:

  • Hyperhomocysteinemia exacerbates cardiac remodeling in rats by promoting oxidative stress and inhibiting the Nrf2/HO-1 pathway.
  • Hypertension amplifies the detrimental effects of HHcy on cardiac remodeling, underscoring the synergistic negative impact of these conditions.
  • The findings reveal a critical role for the Nrf2/HO-1 pathway and oxidative stress in the pathogenesis of cardiac remodeling induced by HHcy and hypertension.
Abstract

Keywords:
Cardiac remodelingHHcyHO-1HypertensionNrf2

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