{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T21:58:15Z","timestamp":1781301495375,"version":"3.54.1"},"reference-count":66,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["OMICS: A Journal of Integrative Biology"],"published-print":{"date-parts":[[2026,5,1]]},"abstract":"<jats:p>\n                    Muscular dystrophies (MDs) are inherited neuromuscular disorders characterized by progressive muscle degeneration. Although their genetic causes are well known, the contribution of autoimmune diseases to MD risk remains unclear. To address this gap, we performed a bidirectional two-sample Mendelian randomization (2SMR) analysis to investigate the potential causal relationship between genetic liability to 21 autoimmune diseases and MD. Genome-wide significant single-nucleotide polymorphisms (\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    &lt; 5 \u00d7 10\n                    <jats:sup>\u22128<\/jats:sup>\n                    ) were used as instrumental variables. The primary analysis employed inverse-variance weighting, complemented by MR-Egger, weighted median, and weighted mode methods, alongside extensive sensitivity analyses. Our results indicate that five autoimmune conditions demonstrated statistically significant associations with MD. Genetic liability to ankylosing spondylitis (odds ratio [OR] = 0.86, 95% confidence interval [CI]: 0.78\u20130.95,\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    = 1.91 \u00d7 10\n                    <jats:sup>\u22123<\/jats:sup>\n                    ), multiple sclerosis (OR = 0.55, 0.38\u20130.79,\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    = 1.36 \u00d7 10\n                    <jats:sup>\u22123<\/jats:sup>\n                    ), ulcerative colitis (OR = 0.57, 0.42\u20130.77,\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    = 2.54 \u00d7 10\n                    <jats:sup>\u22124<\/jats:sup>\n                    ), and rheumatoid arthritis (RA) (OR = 0.65, 95% CI: 0.51\u20130.86,\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    = 7.01 \u00d7 10\n                    <jats:sup>\u22124<\/jats:sup>\n                    ) was associated with a lower risk of MD, whereas genetic liability to asthma showed a positive association with MD risk (OR = 2.18, 95% CI: 1.18\u20134.00,\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    = 1.17 \u00d7 10\n                    <jats:sup>\u22123<\/jats:sup>\n                    ). Per-disease Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses further supported these findings by revealing condition-specific enrichment in immune-related pathways, with the strongest signals observed for RA and asthma through shared HLA class II-driven Th17 and Th1\/Th2 differentiation pathways. These findings should be interpreted cautiously given that the MD outcome of genome-wide association study comprised 242 cases and represents a composite phenotype encompassing multiple genetically distinct subtypes. This study provides novel genetic evidence that genetic liability to specific autoimmune diseases is differentially associated with MD risk, highlighting immune-related pathways that may contribute to neuromuscular pathobiology.\n                  <\/jats:p>","DOI":"10.1177\/15578100261451560","type":"journal-article","created":{"date-parts":[[2026,5,23]],"date-time":"2026-05-23T12:44:59Z","timestamp":1779540299000},"page":"271-283","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Uncovering Causal Links Between Autoimmune Diseases and Muscular Dystrophy: A Bidirectional Mendelian Randomization Study"],"prefix":"10.1177","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-6353-9505","authenticated-orcid":false,"given":"Aytac","family":"Gul","sequence":"first","affiliation":[{"name":"Department of Medical Biology, Tayfur Ata S\u00f6kmen Faculty of Medicine, Hatay Mustafa Kemal University, Hatay, T\u00fcrkiye."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tugba","family":"Calisir","sequence":"additional","affiliation":[{"name":"Department of Neurology, Tayfur Ata S\u00f6kmen Faculty of Medicine, Hatay Mustafa Kemal University, Hatay, T\u00fcrkiye."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hamdi","family":"Oguzman","sequence":"additional","affiliation":[{"name":"Department of Medical Biochemistry, Tayfur Ata S\u00f6kmen Faculty of Medicine, Hatay Mustafa Kemal University, Hatay, T\u00fcrkiye."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,5,23]]},"reference":[{"key":"e_1_3_3_2_1","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2014.00491"},{"key":"e_1_3_3_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/ana.24370"},{"key":"e_1_3_3_4_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.2517-6161.1995.tb02031.x"},{"key":"e_1_3_3_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng.3434"},{"key":"e_1_3_3_6_1","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2020.573347"},{"issue":"12","key":"e_1_3_3_7_1","first-page":"2681","article-title":"Invited commentary: Detecting individual and global horizontal pleiotropy in mendelian randomization-A job for the humble heterogeneity statistic","volume":"187","author":"Bowden J","year":"2018","unstructured":"Bowden J, , Hemani G, , Davey Smith G. 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