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Background Finding effective and safe therapeutic drugs for atrial fibrillation (AF) is an important concern for clinicians. Proteome‐wide Mendelian randomization analysis provides new ideas for finding potential drug targets. Methods and Results Using a proteome‐wide Mendelian randomization approach, we assessed the genetic predictive causality between thousands of proteins and AF risk and found that genetically predicted plasma levels of phosphomevalonate kinase, tumor necrosis factor ligand superfamily member 12, sulfhydryl oxidase 2, interleukin‐6 receptor subunit alpha, and low‐affinity immunoglobulin gamma Fc region receptor II‐b might decrease AF risk, while genetically predicted plasma levels of beta‐mannosidase, collagen alpha‐1(XV) chain, ANXA4 (annexin A4), COF2 (cofilin‐2), and RAB1A (Ras‐related protein Rab‐1A) might increase AF risk (P |
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