ArticleLipids in health and disease2025
Arachidonic acid is involved in high-salt diet-induced coronary remodeling through stimulation of the IRE1α/XBP1s/RUNX2/OPN signaling cascade.
Article in Lipids in health and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Plasma metabolic profiling reveals exploratory metabolic differences in chronic coronary syndrome with coronary artery calcification.Frontiers in cardiovascular medicine · 2026Article
- The interaction between COX-2 and endoplasmic reticulum stress is involved in liver ischemia-reperfusion injury in mice.Molecular biology reports · 2025Article
- Mode and Mechanism of Action of Omega-3 and Omega-6 Unsaturated Fatty Acids in Chronic Diseases.Nutrients · 2025Review
- Targeting of arachidonic acid-modulated autophagy to enhance the sensitivity ofTranslational lung cancer research · 2025Article
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7 authors.
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Abstract
backgroundThe impact of a high-salt (HS) diet on metabolic disturbances in individuals with coronary heart disease remains unclear. The arachidonic acid (AA) metabolic pathway is closely linked to the development of cardiometabolic diseases and atherosclerotic cardiovascular diseases. Furthermore, endoplasmic reticulum stress (ERS) has emerged as a major contributor to cardiometabolic diseases. AA-related inflammation and ERS are hypothesized to play a role in HS diet-induced coronary remodeling.
methodsRats were subjected to an HS diet for 4 weeks, and the serum concentration of AA was measured via enzyme-linked immunosorbent assay. Immunofluorescence staining and vascular tension measurements were conducted on coronary arteries. In addition, AA-stimulated coronary artery smooth muscle cells (CASMCs) were treated with ERS inhibitors to explore the underlying pathway involved.
resultsIncreased susceptibility to myocardial infarction in the HS diet-fed rats was accompanied by increased serum AA concentrations and increased expression of the key AA metabolic enzyme cyclooxygenase-2 (COX-2). AA incubation weakened the contraction of denuded coronary arteries, reduced the expression of contraction markers, and increased the fluorescence intensity of synthetic and ERS response markers in coronary arteries. Further investigation of CASMCs revealed that AA-induced phenotypic transformation was mediated via the ERS pathway.
conclusionsERS and AA were found to be stimulated in CASMCs following an HS diet. AA triggers an ERS response through COX-2 catalysis, and the downstream inositol requiring enzyme 1 - X-box binding protein-1 - osteopontin pathway may contribute to the AA-induced phenotypic transformation of CASMCs, resulting in dysfunctional coronary tension. This study may provide potential therapeutic targets for cardiovascular diseases associated with excessive AA-derived ERS.
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