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IMNM pathogenesis is unclear. This study investigated key biomarkers and potential pathways for IMNM using high-throughput sequencing and bioinformatics technology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec sec-type=\"materials-methods\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      RNA sequencing was conducted in 18 IMNM patients and 10 controls. A combination of weighted gene coexpression network analysis (WGCNA) and differentially expressed gene (DEG) analysis was conducted to identify IMNM-related DEGs. Feature genes were screened out by employing the protein\n                      <jats:private-char name=\"sbnd\"\/>\n                      protein interaction (PPI) network, support vector machine-recursive feature elimination (SVM-RFE), and least absolute shrinkage selection operator (LASSO). Quantitative real-time polymerase chain reaction (qRT\n                      <jats:private-char name=\"sbnd\"\/>\n                      PCR) was performed to verify their differential expression, and the receiver operating characteristic curve (ROC) was used to evaluate their diagnostic efficiency. Functional enrichment analysis was applied to reveal the hidden functions of feature genes. Furthermore, 28 immune cell abundance patterns in IMNM samples were measured.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec sec-type=\"results\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified 193 IMNM-related DEGs that were aberrantly upregulated in the IMNM population and were closely associated with immune-inflammatory responses, regulation of skeletal and cardiac muscle contraction, and lipoprotein metabolism. With the help of the PPI network and the LASSO and SVM-RFE algorithms, three feature genes,\n                      <jats:italic toggle=\"yes\">LTK<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">MYBPH<\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">MYL4,<\/jats:italic>\n                      were identified and further confirmed by qRT\n                      <jats:private-char name=\"sbnd\"\/>\n                      PCR. ROC curves among IMNM, dermatomyositis (DM), inclusion body myositis (IBM), and polymyositis (PM) samples validated the\n                      <jats:italic toggle=\"yes\">LTK<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">MYL4<\/jats:italic>\n                      genes as IMNM-specific feature markers. In addition, all three genes had a notable association with the autophagy\n                      <jats:private-char name=\"sbnd\"\/>\n                      lysosome pathway and immune-inflammatory responses. Ultimately, IMNM displayed a marked immune-cell infiltrative microenvironment. The most significant correlation was found between CD4 T cells, CD8 T cells, macrophages, natural killer (NK) cells, and dendritic cells (DCs).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec sec-type=\"conclusion\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">LTK<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">MYBPH<\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">MYL4<\/jats:italic>\n                      were identified as potential key molecules for IMNM and are believed to play a role in the autophagy\n                      <jats:private-char name=\"sbnd\"\/>\n                      lysosome pathway and muscle inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1016\/j.csbj.2023.03.019","type":"journal-article","created":{"date-parts":[[2023,3,15]],"date-time":"2023-03-15T12:58:56Z","timestamp":1678885136000},"page":"2228-2240","update-policy":"https:\/\/doi.org\/10.1016\/elsevier_cm_policy","source":"Crossref","is-referenced-by-count":13,"title":["Identification of feature genes and key biological pathways in immune-mediated necrotizing myopathy: High-throughput sequencing and bioinformatics analysis"],"prefix":"10.34133","volume":"21","author":[{"given":"Kai","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Neurology, Sichuan Academy of Medical Science and Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China, Chengdu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chun-yan","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Neurology, Sichuan Academy of Medical Science and Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China, Chengdu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia-ying","family":"Bai","sequence":"additional","affiliation":[{"name":"Department of Neurology, Sichuan Academy of Medical Science and Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China, Chengdu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feng","family":"Xiao","sequence":"additional","affiliation":[{"name":"Department of Neurology, Sichuan Academy of Medical Science and Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China, Chengdu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Song","family":"Tan","sequence":"additional","affiliation":[{"name":"Department of Neurology, Sichuan Academy of Medical Science and Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China, Chengdu, China"},{"name":"Sichuan Provincial Key Laboratory for Human Disease Gene Study, Chengdu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiao","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Immunology, Sichuan Academy of Medical Science and Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China, Chengdu, China"},{"name":"Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China, Chengdu, China,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Neurology, Sichuan Academy of Medical Science and Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China, Chengdu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"221","published-online":{"date-parts":[[2023,3,28]]},"reference":[{"key":"e_1_3_5_2_2","doi-asserted-by":"crossref","first-page":"337","DOI":"10.1016\/j.nmd.2004.02.006","article-title":"119th Enmc international workshop: trial design in adult idiopathic inflammatory myopathies, with the exception of inclusion body myositis, 10\u201312 october 2003, Naarden, the Netherlands","volume":"14","author":"Hoogendijk J.E.","year":"2004","unstructured":"Hoogendijk J.E., Amato A.A., Lecky B.R., Choy E.H., Lundberg I.E., Rose M.R. et al: 119th Enmc international workshop: trial design in adult idiopathic inflammatory myopathies, with the exception of inclusion body myositis, 10\u201312 october 2003, Naarden, the Netherlands. 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