Hyperhomocysteinemia-Induced Oxidative Stress Aggravates Renal Damage in Hypertensive Rats

Ning Gao1, Yuzhen Zhang2, Li Li3

  • 1Department of Cardiology, The First Affiliated Hospital of Shandong First Medical University, Jinan, Shandong, China.

Insights

Hyperhomocysteinemia (HHcy) exacerbates hypertensive renal damage by increasing oxidative stress. This study investigated the synergistic effects of HHcy and hypertension on kidney injury in rats.

Area of Science:

  • Nephrology
  • Cardiovascular Research
  • Oxidative Stress Biology

Background:

  • Hyperhomocysteinemia (HHcy) is known to synergize with hypertension in vascular injury.
  • The specific role of HHcy in hypertension-related renal injury and its underlying mechanisms require further elucidation.

Purpose of the Study:

  • To investigate the relationship between HHcy and hypertension in the context of renal injury.
  • To elucidate the mechanism by which HHcy and hypertension interact to cause renal damage.

Main Methods:

  • Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR) were subjected to hyperhomocysteinemia (HHcy).
  • Evaluated blood pressure, plasma homocysteine, oxidative stress markers (MDA, SOD), renal function (UACR, GFR), and kidney histopathology.
  • Assessed expression of NOX2, NOX4, and nephrin in renal tissue.

Main Results:

  • HHcy and hypertension significantly increased oxidative stress markers (MDA) and decreased antioxidant capacity (SOD) and GFR.
  • Elevated UACR and increased glomerular extracellular matrix were observed in HHcy and hypertensive groups.
  • Renal expression of NOX2 and NOX4 was upregulated, while nephrin expression was downregulated.

Conclusions:

  • Hyperhomocysteinemia synergistically exacerbates hypertensive renal damage.
  • Oxidative stress is a key mechanism mediating the combined detrimental effects of HHcy and hypertension on the kidney.
Abstract

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