动脉僵硬和肌肉减少症的因果关系:孟德尔随机分析。

Hengjun Liu, Tianwei Meng, Rui Qie
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引用次数: 0

摘要

观察性研究和临床试验表明动脉僵硬(AS)和肌肉减少症(SAR)之间存在联系,但两者之间的因果关系尚不清楚。本研究旨在通过孟德尔随机化(MR)研究AS与SAR之间的因果关系。我们分析了全基因组关联研究数据的AS指标:脉搏波动脉僵硬指数(PWASI)和脉搏波峰至峰时间(PPT),以及SAR指标:低握力(LHGS)、通常步行速度(UWP)、中高强度身体活动水平(MVPA)和步行或骑车10分钟。对mr应用方差加权逆、MR-Egger、加权模式和加权中位数。AS与SAR之间存在双向因果关系。PWASI与UWP之间存在因果关系(比值比[OR] = 0.97, 95%可信区间[CI] = 0.94-0.99)。PPT与MVPA (OR = 1.08, 95% CI = 1.002-1.144)和UWP (OR = 1.05, 95% CI = 1.017-1.096)有因果关系。LHGS与PPT有因果关系(OR = 0.95, 95% CI = 0.91-0.98), UWP与PWASI (OR = 0.77, 95% CI = 0.65-0.90)和PPT有因果关系(OR = 1.37, 95% CI = 1.17-1.60)。AS的增加可使运动能力轻度降低,而下肢、上肢力量的增加可导致AS的升高。这两者的双向因果关系可能为促进对与AS和肌肉病理生理相关的潜在机制的理解提供新的视角。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Causal Associations with Arterial Stiffness and Sarcopenia: A Mendelian Randomization Analysis.

Observational studies and clinical trials indicate a link between arterial stiffness (AS) and sarcopenia (SAR), yet the causal relationship between these remains unclear. The study aims to investigate the causal connection from AS to SAR by Mendelian randomization (MR). We analyzed Genome-Wide Association Studies data for AS indicators: pulse wave arterial stiffness index (PWASI) and pulse wave peak-to-peak time (PPT), and SAR indicators: low hand grip strength (LHGS), usual walking pace (UWP), moderate-to-vigorous physical activity levels (MVPA), and walk or cycle unassisted for 10 minutes. The inverse variance-weighted, MR-Egger, weighted mode, and weighted median were applied to MR. There is a bidirectional causal relationship between the AS and SAR. The PWASI has a causation with UWP (odds ratio [OR] = 0.97, 95% confidence interval [CI] = 0.94-0.99). The PPT has a causal association with MVPA (OR = 1.08, 95% CI = 1.002-1.144) and UWP (OR = 1.05, 95% CI = 1.017-1.096). The LHGS is causally associated with PPT (OR = 0.95, 95% CI = 0.91-0.98) and UWP has a causal association with PWASI (OR = 0.77, 95% CI = 0.65-0.90) and PPT (OR = 1.37, 95% CI = 1.17-1.60). The increased AS could reduce the motor ability slightly and the lower upper and lower limb strength could lead to the higher AS. This bidirectional causal relationship of the two may offer novel perspectives for advancing the understanding of the underlying mechanisms related to AS and muscle pathophysiology.

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