Evaluating the causal effect of atherosclerosis on the risk of intervertebral disc degeneration

Author:

Cai Yang‐Ting123,Zhong Xian‐Xing23,Mo Ling23,Huang Rui‐Ze1,Lin Qiang1,Liu Cai‐Jun23ORCID,Zhang Shun‐Cong1ORCID

Affiliation:

1. Guangzhou University of Chinese Medicine Guangzhou People's Republic of China

2. The Third Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou People's Republic of China

3. Guangdong Research Institute for Orthopedics & Traumatology of Chinese Medicine Guangzhou People's Republic of China

Abstract

AbstractBackgroundIntervertebral disc degeneration (IDD) and atherosclerosis are two common age‐related conditions that can cause significant morbidity. While previous studies have suggested an association between the two conditions, the nature of this association remains unclear.MethodsWe used Mendelian randomization (MR) to investigate the causal relationship between IDD and atherosclerosis. We identified genetic variants associated with IDD using summary statistics from a large genome‐wide association study (GWAS). These variants were then used as instrumental variables to infer causal relationships with atherosclerosis in summary statistics from a separate GWAS.ResultsOur MR analysis provided evidence for a causal relationship between IDD and atherosclerosis. We found that the genetic predisposition to atherosclerosis was associated with a higher risk of IDD (odds ratio [OR] = 3.55, 95% confidence interval [CI]: 1.07–11.74, p = 0.04). The IVW estimates were consistent with the observational findings and other robust MR methods. Sensitivity analyses suggested that our findings were robust to potential sources of bias.ConclusionsOur study provides evidence for a causal link between IDD and atherosclerosis, suggesting that interventions targeting atherosclerosis could have potential benefits for reducing the risk of IDD. Further research is needed to explore the underlying mechanisms that link these two conditions and to investigate potential therapeutic interventions.

Publisher

Wiley

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