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High Uric Acid Inhibits Cardiomyocyte Viability Through the ERK/P38 Pathway via Oxidative Stress

Zhi Li1, Yang Shen2, Yingqun Chen1,3

  • 1Department of Internal Medicine, The Second Affiliated Hospital of Shantou, University Medical College, Shantou, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|February 15, 2018
PubMed

Insights

High uric acid (HUA) damages heart cells by increasing oxidative stress and activating specific signaling pathways. This study reveals a novel mechanism linking HUA to cardiovascular disease through ERK/p38 activation.

Area of Science:

  • Cardiovascular Biology
  • Cellular Signaling
  • Oxidative Stress Research

Background:

  • Hyperuricemia is linked to cardiovascular disease, but underlying mechanisms are unclear.
  • Understanding high uric acid's impact on heart cells is crucial for disease prevention.

Purpose of the Study:

  • Investigate the effects of high uric acid (HUA) on cardiomyocytes.
  • Elucidate the molecular pathways involved in HUA-induced cardiac dysfunction.

Main Methods:

  • H9c2 cardiomyocytes exposed to HUA; viability assessed via MTT assay.
  • Reactive oxygen species (ROS) production measured using fluorescence assays.
  • Western blotting analyzed key signaling proteins (ERK, p38, PI3K, Akt); mouse model used.

Main Results:

  • HUA reduced cardiomyocyte viability and increased ROS production.
  • ROS scavenger and ERK inhibitor partially restored cell viability.
  • HUA activated ERK/p38 and inhibited PI3K/Akt signaling in cardiomyocytes and mouse models.

Conclusions:

  • HUA induces oxidative damage and impairs cardiomyocyte viability.
  • Activation of ERK/p38 signaling is a key mechanism in HUA-induced cardiac damage.
  • This provides a novel molecular insight into hyperuricemia-related cardiovascular disease.
Abstract

Keywords:
CardiomyocytesHigh uric acidInhibitionOxidative stress

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