Scholarlink

Background <p>Previous studies have indicated the association between cardiovascular disease (CVD), cancer and lipid, while the causality remain unclear. We aim to elucidate the causality among them and potential mediating factors.</p> Methods <p>We extracted datasets on CVD, cancer and lipid from the Genome-Wide Association Study (GWAS) database. Univariate and multivariate Mendelian Randomization (MR) analyses were employed to assess the causal relationships among them. Potential interactions were explored through mediation analysis. Sensitivity analysis was performed to ensure the robustness.</p> Results <p>In the univariate MR analysis, all CVDs demonstrated a negative causal relationship with at least one type of cancer (all <i>P</i> &lt; 0.05). The reverse MR analysis indicated that other cancers exhibited a negative causal relationship with at least one CVD, except for lung, prostate or thyroid cancer (all <i>P</i> &lt; 0.05). Regarding the effect of lipids on CVDs, high density lipoprotein cholesterol (HDL-C) and apolipoprotein A1 (ApoA1) were found to be negatively correlated with CVDs (all <i>P</i> &lt; 0.05), while other lipids showed a positive relationship (all <i>P</i> &lt; 0.05). Notably, most lipids are negatively causally associated with cancers (all <i>P</i> &lt; 0.05). Mediation analysis confirmed that CVD mediates the causal relationship between lipids and cancers.</p> Conclusion <p>This study explored the pairwise causal relationships among lipid, CVD, and cancer from a genetic perspective. However, the identified inverse causal associations should be interpreted as effects at the genetic level, rather than as evidence supporting CVD as a direct preventive strategy against cancer in clinical practice. Nonetheless, these findings inspire further investigation into novel biological mechanisms linking CVD and cancer, with the potential to identify new anticancer strategies.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Elucidating the causal triad of cardiovascular disease, cancer, and lipid traits: a bidirectional Mendelian randomization study with genetic mediation analysis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月14日

查看全文
  • Weijie Wu,
  • Aiming Zeng,
  • Yunzhe Yu,
  • Liqun Liao,
  • Yuheng Jiao,
  • Jiaqi Hu,
  • Jiansheng Chen

摘要

Background

Previous studies have indicated the association between cardiovascular disease (CVD), cancer and lipid, while the causality remain unclear. We aim to elucidate the causality among them and potential mediating factors.

Methods

We extracted datasets on CVD, cancer and lipid from the Genome-Wide Association Study (GWAS) database. Univariate and multivariate Mendelian Randomization (MR) analyses were employed to assess the causal relationships among them. Potential interactions were explored through mediation analysis. Sensitivity analysis was performed to ensure the robustness.

Results

In the univariate MR analysis, all CVDs demonstrated a negative causal relationship with at least one type of cancer (all P < 0.05). The reverse MR analysis indicated that other cancers exhibited a negative causal relationship with at least one CVD, except for lung, prostate or thyroid cancer (all P < 0.05). Regarding the effect of lipids on CVDs, high density lipoprotein cholesterol (HDL-C) and apolipoprotein A1 (ApoA1) were found to be negatively correlated with CVDs (all P < 0.05), while other lipids showed a positive relationship (all P < 0.05). Notably, most lipids are negatively causally associated with cancers (all P < 0.05). Mediation analysis confirmed that CVD mediates the causal relationship between lipids and cancers.

Conclusion

This study explored the pairwise causal relationships among lipid, CVD, and cancer from a genetic perspective. However, the identified inverse causal associations should be interpreted as effects at the genetic level, rather than as evidence supporting CVD as a direct preventive strategy against cancer in clinical practice. Nonetheless, these findings inspire further investigation into novel biological mechanisms linking CVD and cancer, with the potential to identify new anticancer strategies.