<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Meng S</submitter><funding>Sanming Project of Medicine in Shenzhen</funding><funding>Shenzhen Key Medical Discipline Construction Fund</funding><pagination>123-137</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9830643</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>22(1)</volume><pubmed_abstract>Dermatomyositis and polymyositis (DM/PM) are systemic autoimmune diseases characterized by proximal muscle weakness. The underlying pathogenetic mechanism of this disease remains under-researched. Here, using proteomics analysis, a great overlap of differentially expressed plasma exosomal proteins involved in the complement and coagulation cascade pathway, including FGA, FGB, FGG, C1QB, C1QC, and VWF, was identified in DM/PM patients versus healthy controls. Correlation analysis showed that the expression levels of complement-associated proteins (C1QB and C1QC) correlated positively with CRP, ESR, and platelet count. ROC curve analysis demonstrated that complement and coagulation cascade-associated proteins could be strong predictors for DM/PM. In addition, we also identified several other proteins that were differentially expressed in DM and PM. The selected candidate proteins were further validated by parallel reaction monitoring (PRM) and enzyme-linked immunosorbent assay (ELISA). Together, our findings indicate that these exosome-derived proteins might participate in microvascular damage in DM/PM through the activation of the complement and coagulation cascade pathway and function as biomarkers for the clinical diagnosis of DM/PM.</pubmed_abstract><journal>Journal of proteome research</journal><pubmed_title>Proteomics Analysis of Plasma-Derived Exosomes Unveils the Aberrant Complement and Coagulation Cascades in Dermatomyositis/Polymyositis.</pubmed_title><pmcid>PMC9830643</pmcid><funding_grant_id>SZXK011</funding_grant_id><funding_grant_id>SZSM202111006</funding_grant_id><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Meng S</pubmed_authors><pubmed_authors>Hong X</pubmed_authors><pubmed_authors>Zhao Q</pubmed_authors><pubmed_authors>Wang T</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Liu C</pubmed_authors><pubmed_authors>Hu Q</pubmed_authors><pubmed_authors>Liu D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Proteomics Analysis of Plasma-Derived Exosomes Unveils the Aberrant Complement and Coagulation Cascades in Dermatomyositis/Polymyositis.</name><description>Dermatomyositis and polymyositis (DM/PM) are systemic autoimmune diseases characterized by proximal muscle weakness. The underlying pathogenetic mechanism of this disease remains under-researched. Here, using proteomics analysis, a great overlap of differentially expressed plasma exosomal proteins involved in the complement and coagulation cascade pathway, including FGA, FGB, FGG, C1QB, C1QC, and VWF, was identified in DM/PM patients versus healthy controls. Correlation analysis showed that the expression levels of complement-associated proteins (C1QB and C1QC) correlated positively with CRP, ESR, and platelet count. ROC curve analysis demonstrated that complement and coagulation cascade-associated proteins could be strong predictors for DM/PM. In addition, we also identified several other proteins that were differentially expressed in DM and PM. The selected candidate proteins were further validated by parallel reaction monitoring (PRM) and enzyme-linked immunosorbent assay (ELISA). Together, our findings indicate that these exosome-derived proteins might participate in microvascular damage in DM/PM through the activation of the complement and coagulation cascade pathway and function as biomarkers for the clinical diagnosis of DM/PM.</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-04T07:21:16.907Z</modification><creation>2025-04-04T07:21:16.907Z</creation></dates><accession>S-EPMC9830643</accession><cross_references><pubmed>36507906</pubmed><doi>10.1021/acs.jproteome.2c00532</doi></cross_references></HashMap>