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The short-chain fatty acid propionate prevents ox-LDL-induced coronary microvascular dysfunction by alleviating

Dan Hong1, Wen Tang1, Fei Li1

  • 1Department of Geriatric Medicine, Xiangya Hospital, Central South University, Hunan, China.

Plos One
|May 30, 2024
PubMed

Insights

Oxidized low-density lipoprotein (ox-LDL) triggers coronary microvascular dysfunction (CMD) by inducing endoplasmic reticulum (ER) stress. Short-chain fatty acid propionate protects against this by inhibiting ER stress and restoring nitric oxide production.

Area of Science:

  • Cardiovascular Biology
  • Endothelial Cell Function
  • Gut Microbiome Metabolites

Background:

  • Coronary microvascular dysfunction (CMD) is a key factor in cardiovascular diseases, often linked to reduced nitric oxide (NO) generation due to lower endothelial nitric oxide synthase (eNOS) phosphorylation.
  • Endoplasmic reticulum (ER) stress is known to impair NO production in endothelial cells, and oxidized low-density lipoprotein (ox-LDL) damages endothelial function, but their combined role in coronary microcirculation was unclear.

Purpose of the Study:

  • To investigate the impact of ox-LDL on coronary microcirculation and the potential protective role of short-chain fatty acids (SCFAs).
  • To elucidate the underlying mechanisms of ox-LDL-induced endothelial dysfunction and the therapeutic potential of propionate.

Main Methods:

  • Human cardiac microvascular endothelial cells were treated with ox-LDL to assess ER stress markers and signaling pathways (PERK/eIF2a, IRE1/JNK, ATF6).
  • The effects on eNOS phosphorylation and NO production were measured.
  • The impact of SCFA-propionate on these ox-LDL-induced changes was evaluated.

Main Results:

  • Ox-LDL significantly increased ER chaperone GRP78 expression and activated downstream ER stress signaling pathways in cardiac microvascular endothelial cells.
  • This activation led to decreased eNOS phosphorylation and reduced NO production, indicative of CMD.
  • Propionate effectively inhibited ox-LDL-induced ER stress and its downstream signaling, thereby restoring eNOS phosphorylation and NO production.

Conclusions:

  • Ox-LDL induces coronary microvascular dysfunction by activating ER stress pathways in cardiac endothelial cells.
  • Short-chain fatty acid propionate demonstrates a protective effect against ox-LDL-induced endothelial dysfunction.
  • Propionate counteracts the adverse effects of ox-LDL by inhibiting ER stress, offering a potential therapeutic strategy for protecting coronary microcirculation.

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