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Ganoderma triterpenes Protect Against Hyperhomocysteinemia Induced Endothelial-Mesenchymal Transition via TGF-β

Jinzhao He1, Yi Sun1, Yingli Jia1

  • 1Key Laboratory of Molecular Cardiovascular Sciences, State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China.

Frontiers in Physiology
|March 21, 2019
PubMed

Insights

Hyperhomocysteinemia causes endothelial-mesenchymal transition (EndMT) by activating key signaling pathways. Ganoderma triterpenes (GT) show protective effects against this process by reducing oxidative stress and inhibiting these pathways.

Area of Science:

  • Cardiovascular Biology
  • Cellular Mechanisms
  • Pharmacology

Background:

  • Endothelial dysfunction is a critical factor in cardiovascular diseases linked to hyperhomocysteinemia (HHcy).
  • The precise mechanisms of HHcy-induced endothelial injury and effective treatments remain unclear.
  • Endothelial-mesenchymal transition (EndMT) is implicated in HHcy-related pathologies.

Purpose of the Study:

  • To investigate the mechanisms underlying HHcy-induced endothelial injury.
  • To explore the protective potential of Ganoderma triterpenes (GT) against HHcy-induced endothelial damage.
  • To elucidate the signaling pathways involved in HHcy-induced EndMT.

Main Methods:

  • Utilized bovine aortic endothelial cells (BAECs) as an in vitro model.
  • Employed small molecular inhibitors to probe signaling pathways (TGF-β/Smad, PI3K/AKT, MAPK).
  • Assessed the effects of Ganoderma triterpenes (GT) on HHcy-induced EndMT, oxidative stress, and pathway activation.

Main Results:

  • Hyperhomocysteinemia (HHcy) induced endothelial-mesenchymal transition (EndMT) in BAECs.
  • Activation of TGF-β/Smad, PI3K/AKT, and MAPK signaling pathways was observed during HHcy-induced EndMT.
  • Ganoderma triterpenes (GT) inhibited HHcy-induced EndMT by reducing oxidative stress and suppressing these signaling pathways, including Snail activity.

Conclusions:

  • HHcy induces EndMT through the activation of TGF-β/Smad, PI3K/AKT, and MAPK pathways.
  • Ganoderma triterpenes (GT) demonstrate therapeutic potential for HHcy-induced EndMT.
  • GT alleviates oxidative stress and inhibits key signaling pathways, offering a novel treatment strategy.

Keywords:
Ganoderma triterpenesTGF-βendothelial cellsendothelial-mesenchymal transitionhomocysteineoxidative stress

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