AI Article Synopsis
- Mitochondrial dysfunction, particularly a deficiency in complex I, has been linked to coronary artery disease (CAD) and is implicated in various cardiovascular issues, including acute coronary syndrome (ACS).
- A study involving 260 CAD patients found that the T allele of the /rs23117379 genetic variant is associated with an earlier onset of ACS and a higher risk of recurrence.
- The findings suggest that this genetic variant may serve as a potential risk factor for cardiovascular diseases due to its role in mitochondrial dysfunction.
Article Abstract
Background: Among several potential mechanisms, mitochondrial dysfunction has been proposed to be involved in the pathogenesis of coronary artery disease (CAD). A mitochondrial complex I deficiency severely impairs cardiovascular health and contributes to CAD development. Previous evidence highlighted a key role of , a subunit of complex I, deficiency in the increased occurrence of renal and cerebrovascular damage in an animal model of hypertension, and of juvenile ischemic stroke occurrence in humans. Furthermore, a significant decrease of mRNA was detected in peripheral blood mononuclear cells from patients experiencing acute coronary syndrome (ACS). The T allele at /rs23117379 variant is known to associate with reduced gene expression and mitochondrial dysfunction.
Objective: In the present study we tested the impact of the T/C /rs23117379 variant on occurrence of ACS in a prospective cohort of CAD patients ( = 260).
Results: Hypertension, smoking habit, diabetes and hypercholesterolemia were present in a large proportion of patients. Non-ST-elevation myocardial infarction (NSTEMI) represented the most frequent type of ACS (44%, = 115), followed by ST-elevation myocardial infarction (STEMI) (34%, = 88) and unstable angina (22%, = 57). The alleles/genotypes distribution for T/C at /rs23117379 revealed that the TT genotype was associated with a trend toward the development of ACS at an earlier age (TT 61 ± 12, CT 65 ± 12 and CC 66 ± 11 years; = 0.051 after adjustment for gender, hypertension, smoking habit, diabetes and hypercholesterolemia) and with a significant predictive role for ACS recurrence (hazard ratio [HR]1.671; 95% confidence interval [CI], 1.138-2.472; = 0.009).
Conclusions: Our findings are consistent with a deleterious effect of deficiency on acute coronary events predisposition and further support a role of the /rs23117379 variant as a genetic cardiovascular risk factor.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9197441 | PMC |
| http://dx.doi.org/10.3389/fcvm.2022.921244 | DOI Listing |
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