This study explores the relationship between iron metabolism and multiple sclerosis (MS) through integrated bioinformatics analysis and Mendelian randomization (MR) methods. The research identifies several genes associated with MS and iron metabolism, including IREB2, LAMP2, ISCU, ATP6V1G1, ATP13A2, and SKP1, which demonstrate multi-gene diagnostic value for MS with an area under the curve (AUC) of 0.83. MR analysis reveals a potential causal relationship between transferrin saturation and MS (p=2.22E-02; OR 95% CI=0.86 (0.75, 0.98)), as well as serum transferrin and MS (p=2.18E-04; OR 95% CI=1.22 (1.10, 1.36)). The findings suggest that iron metabolism disorder may play an important role in the pathogenesis of MS. The study also highlights the complex interplay between iron and MS, providing important insights for further research into the role of iron metabolism in MS and offering crucial theoretical support for the treatment of MS. The study used publicly available databases and bioinformatics techniques for gene expression data analysis, including differential expression analysis, weighted correlation network analysis, gene enrichment analysis, and construction of logistic regression models. Subsequently, MR was used to assess the causal relationship between different iron metabolism markers and MS. The study's results provide new evidence for further research on the pathogenic mechanism of iron in MS. The study also found that iron deficiency may impact the pathophysiological processes in MS patients, including affecting the health and regeneration of oligodendrocytes and myelin sheaths. Additionally, iron deficiency may lead to heightened oxidative metabolism activity in oligodendrocytes, as well as impact the synthesis and maintenance of enzymes involved in oxidative metabolism and myelin sheath production. The study's findings suggest that iron metabolism disorder may be an important pathogenic mechanism in MS. The study used comprehensive bioinformatic analysis and MR methods to explore the relationship between iron and MS, aiming to provide new evidence for further research on the pathogenic mechanism of iron in MS. The study's results indicate that iron metabolism may be a key factor in the development and progression of MS. The study also found that iron deficiency may be an important contributing factor to MS. The study's results suggest that iron metabolism disorder may be an important pathogenic mechanism in MS. The study's findings provide important insights for further research into the role of iron metabolism disorder in the pathogenesis of MS and offer crucial theoretical support for the treatment of MS.This study explores the relationship between iron metabolism and multiple sclerosis (MS) through integrated bioinformatics analysis and Mendelian randomization (MR) methods. The research identifies several genes associated with MS and iron metabolism, including IREB2, LAMP2, ISCU, ATP6V1G1, ATP13A2, and SKP1, which demonstrate multi-gene diagnostic value for MS with an area under the curve (AUC) of 0.83. MR analysis reveals a potential causal relationship between transferrin saturation and MS (p=2.22E-02; OR 95% CI=0.86 (0.75, 0.98)), as well as serum transferrin and MS (p=2.18E-04; OR 95% CI=1.22 (1.10, 1.36)). The findings suggest that iron metabolism disorder may play an important role in the pathogenesis of MS. The study also highlights the complex interplay between iron and MS, providing important insights for further research into the role of iron metabolism in MS and offering crucial theoretical support for the treatment of MS. The study used publicly available databases and bioinformatics techniques for gene expression data analysis, including differential expression analysis, weighted correlation network analysis, gene enrichment analysis, and construction of logistic regression models. Subsequently, MR was used to assess the causal relationship between different iron metabolism markers and MS. The study's results provide new evidence for further research on the pathogenic mechanism of iron in MS. The study also found that iron deficiency may impact the pathophysiological processes in MS patients, including affecting the health and regeneration of oligodendrocytes and myelin sheaths. Additionally, iron deficiency may lead to heightened oxidative metabolism activity in oligodendrocytes, as well as impact the synthesis and maintenance of enzymes involved in oxidative metabolism and myelin sheath production. The study's findings suggest that iron metabolism disorder may be an important pathogenic mechanism in MS. The study used comprehensive bioinformatic analysis and MR methods to explore the relationship between iron and MS, aiming to provide new evidence for further research on the pathogenic mechanism of iron in MS. The study's results indicate that iron metabolism may be a key factor in the development and progression of MS. The study also found that iron deficiency may be an important contributing factor to MS. The study's results suggest that iron metabolism disorder may be an important pathogenic mechanism in MS. The study's findings provide important insights for further research into the role of iron metabolism disorder in the pathogenesis of MS and offer crucial theoretical support for the treatment of MS.