» Articles » PMID: 38430243

Cross-sectional Studies of the Causal Link Between Asthma and Osteoporosis: Insights from Mendelian Randomization and Bioinformatics Analysis

Overview
Journal Osteoporos Int
Date 2024 Mar 2
PMID 38430243
Authors
Affiliations
Soon will be listed here.
Abstract

Introduction: Asthma and osteoporosis are prevalent health conditions with substantial public health implications. However, their potential interplay and the underlying mechanisms have not been fully elucidated. Previous research has primarily focused on the impact of glucocorticoids on osteoporosis, often overlooking the role of asthma itself.

Methods: We conducted a multi-stage stratified random sampling in Chongqing, China and excluded individuals with a history of glucocorticoid use. Participants underwent comprehensive health examinations, and their clinical data, including asthma status, were recorded. Logistic regression and Mendelian randomization were employed to investigate the causal link between asthma and osteoporosis. Furthermore, bioinformatics analyses and serum biomarker assessments were conducted to explore potential mechanistic pathways.

Results: We found a significant association between asthma and osteoporosis, suggesting a potential causal link. Mendelian Randomization analysis provided further support for this causal link. Bioinformatics analyses revealed that several molecular pathways might mediate the impact of asthma on bone health. Serum alkaline phosphatase levels were significantly elevated in the asthma group, suggesting potential involvement in bone turnover.

Conclusion: Our study confirms a causal link between asthma and osteoporosis and highlights the importance of considering asthma in osteoporosis prediction models. It also suggests that asthma may accelerate osteoporosis by increasing bone turnover through inflammatory factors, disrupting the coupling between osteoblasts and osteoclasts, ultimately leading to bone loss.

Citing Articles

Mendelian randomization studies of risk and protective factors for osteoporosis: a systematic review and meta-analysis.

Ji W, Pan B, Chen X, Lao Z, Yang W, Qian Y Front Endocrinol (Lausanne). 2025; 15:1486188.

PMID: 39886030 PMC: 11779621. DOI: 10.3389/fendo.2024.1486188.

References
1.
Sims N, Ng K . Implications of osteoblast-osteoclast interactions in the management of osteoporosis by antiresorptive agents denosumab and odanacatib. Curr Osteoporos Rep. 2014; 12(1):98-106. DOI: 10.1007/s11914-014-0196-1. View

2.
Song S, Guo Y, Yang Y, Fu D . Advances in pathogenesis and therapeutic strategies for osteoporosis. Pharmacol Ther. 2022; 237:108168. DOI: 10.1016/j.pharmthera.2022.108168. View

3.
Mundy G . Osteoporosis and inflammation. Nutr Rev. 2008; 65(12 Pt 2):S147-51. DOI: 10.1111/j.1753-4887.2007.tb00353.x. View

4.
Tao H, Li W, Zhang W, Yang C, Zhang C, Liang X . Urolithin A suppresses RANKL-induced osteoclastogenesis and postmenopausal osteoporosis by, suppresses inflammation and downstream NF-κB activated pyroptosis pathways. Pharmacol Res. 2021; 174:105967. DOI: 10.1016/j.phrs.2021.105967. View

5.
Zhang S, Ni W . High systemic immune-inflammation index is relevant to osteoporosis among middle-aged and older people: A cross-sectional study. Immun Inflamm Dis. 2023; 11(8):e992. PMC: 10465993. DOI: 10.1002/iid3.992. View