Key result
Smoking in male CAD patients is linked to ~67% higher ERK 1/2 expression in plaques.
Why the study?
Smoking is a major risk factor for ACS linked to increased MMP activity, but the molecular alterations associated with smoking in ACS remain incompletely understood.
Does smoking alter the expression of α1nAChR, ERK1/2, c-FOS, and matrix metalloproteinases in patients with coronary artery disease?
Observational (n=221)
Does smoking alter the expression of α1nAChR, ERK1/2, c-FOS, and matrix metalloproteinases in patients with coronary artery disease?
Answers are grounded in this paper and cite their sources.
Smoking in patients with coronary artery disease is associated with increased expression of α1nAChR, ERK, and MMP-9, suggesting a molecular mechanism for smoking-induced plaque vulnerability in acute coronary syndrome.
Acute Coronary Syndrome (ACS) is a severe manifestation of Coronary Artery Disease (CAD) caused by the rupture of unstable atherosclerotic plaques, resulting in reduced myocardial blood flow. Smoking is a major risk factor for ACS and has been associated with increased matrix metalloproteinase (MMP) activity, which contributes to the degradation of the plaque fibrous cap. However, the molecular alterations associated with smoking in ACS remain incompletely understood. This study aimed to investigate the expression of α1nAChR, ERK1/2, and c-FOS genes, together with MMP protein levels in atherosclerotic plaque tissues and peripheral blood mononuclear cells (PBMCs) of CAD patients. A total of 41 atherosclerotic plaque samples (26 smokers, 15 non-smokers) and 180 clinical subjects [n = 30 per group: ACS, chronic coronary syndrome (CCS), and controls; smokers and non-smokers] were included. Gene expression of ⍺1nAChR, ERK 1/2, and c-FOS was analyzed by RT-qPCR, while protein levels of MMP-2, MMP-9, and TIMP 3 were measured using ELISA. The expression of ERK 1/2 and c-FOS were significantly higher in plaque tissues of smokers compared with non-smokers (1.671- and 1.327-fold; p < 0.05). In PBMCs, α1nAChR expression was higher in CCS smokers (1.383-fold), while ERK 1/2 expression was higher in ACS smokers (1.355-fold). MMP-9 levels were significantly elevated in ACS and CCS compared with controls (p < 0.001). In conclusion, smoking CAD patients demonstrated increased expression of α1nAChR, ERK and MMP-9, indicating smoking-associated alterations in ⍺1nAChR-ERK signaling-related biomarkers in ACS.
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Samah et al. (2026) conducted an observational in Acute Coronary Syndrome and Coronary Artery Disease (n=221). Smoking vs. Non-smoking was evaluated on Expression of ERK 1/2 and c-FOS in plaque tissues (1.671-fold (ERK 1/2) and 1.327-fold (c-FOS) increase, p=<0.05). Smoking in male CAD patients was associated with increased expression of ERK 1/2 and c-FOS in plaque tissues compared to non-smokers.
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