Further international collaborative research using the specimens from many countries is necessary for the practical use in the world
Further international collaborative research using the specimens from many countries is necessary for the practical use in the world. == Conclusions == Serum DIDO1-Ab, FOXJ2-Ab, and AZ82 CPSF2-Ab appear to be useful for diagnosing AIS AZ82 and may originate from kidney disease, hypertension, and DM, respectively. == Supplementary Information == Additional file 1.Supplementary information. == Acknowledgements == The authors would like to thank Prof. 297311 of DIDO1, 426440 of FOXJ2, and 607621 of CPSF2 to examine serum antibody levels. Compared with HDs, a significant increase in antibody levels of the DIDO1 protein and peptide in patients with AIS, transient ischemic attack (TIA), and chronic kidney disease (CKD) but not in those with acute myocardial infarction and diabetes mellitus (DM). Serum anti-FOXJ2 antibody levels were elevated in most patients with atherosclerosis-related diseases, whereas serum anti-CPSF2 antibody levels were associated with AIS, TIA, and DM. Receiver operating characteristic curves showed that serum DIDO1 antibody levels were highly associated with CKD, and correlation analysis revealed that serum anti-FOXJ2 antibody levels were associated AZ82 with hypertension. A prospective casecontrol study on ischemic stroke verified that this serum antibody levels of the DIDO1 protein and DIDO1, FOXJ2, and CPSF2 peptides showed significantly higher odds ratios with a risk of AIS in patients with the highest quartile than in those with the lowest quartile, indicating that these antibody markers are useful as risk factors for AIS. == Conclusions == Serum antibody levels of DIDO1, FOXJ2, and CPSF2 are useful in predicting the onset of atherosclerosis-related AIS caused by kidney failure, hypertension, and DM, respectively. == Supplementary Information == The online version contains supplementary material available at 10.1186/s12916-021-02001-9. Keywords:Acute ischemic stroke, Antibody biomarker, Atherosclerosis, Acute myocardial infarction, Diabetes mellitus, Chronic kidney disease == Background == Atherosclerosis is usually a serious disease and a major cause of acute ischemic stroke (AIS) and acute myocardial infarction (AMI) [1]. Diabetes mellitus (DM) and chronic kidney disease (CKD) are Capn3 closely related to and accompanied by atherosclerosis [2]. As atherosclerosis progresses, atherosclerotic plaques are formed on artery walls by foam cells, which are differentiated from easy muscle cells or macrophages [35]. Diagnosing atherosclerosis is usually important to prevent the onset of AIS and AMI because the effectiveness of treatment and therapy is limited after their onset. Thus, to date, many risk factors and biomarkers including family history, age, obesity, smoking habit, dyslipidemia, hypertension, sleep, C-reactive protein level, interleukin-6 level, troponin level, and B-type natriuretic peptide level have been reported [6,7]; however, they are still insufficient. Genome-wide association studies on stroke have identified many genes such asNOTCH3[8],CSTA[9], andCOL3A1[10]. However, lifestyle diseases such as stroke and atherosclerosis can be prevented by improving individuals lifestyles. Recent studies have discovered that the development of autoantibodies is not limited to autoimmune diseases but is also observed in other diseases. Some examples include autoantibody markers against proteins such as p53, NY-ESO-1, and RALA for cancer [1114]; Hsp60 for stroke [15]; insulin [16], glutamic acid decarboxylase [17], and protein tyrosine phosphatase IA-2 [18,19] for DM, as well as phospholipid [20], apolipoprotein A1 [21,22], oxidized low-density lipoprotein [22,23], and heat shock proteins [22,24] for AZ82 cardiovascular disease (CVD). Previously, we searched for antibody markers using serological identification of antigens by cDNA expression cloning (SEREX) and the protein array method, and we reported on autoantibodies against Trop2/TACSTD2 [25], TRIM21 [26], Makorin 1 [27], and ECSA [28], for esophageal squamous cell carcinoma; FIR/PUF60 for colon cancer [29]; SH3GL1 [30] and filamin C [31] for glioma; EP300-interacting inhibitor of differentiation 3 for nonfunctional pancreatic neuroendocrine tumors [32]; proline-rich 13 for ulcerative colitis [33]; talin-1 for multiple sclerosis [34]; PSMA7 for amyotrophic lateral sclerosis [35]; NBL1/DAN [36] and SNX16 [37] for obstructive sleep apnea (OSA); and EXD2 for chronic thromboembolic pulmonary hypertension (CTEPH) [38]. We also reported on autoantibody markers for atherosclerosis-related diseases, e.g., RPA2 [39], PDCD11 [40], MMP1 [41], and DNAJC2 [42] for AIS; ASXL2 [43] for atherosclerosis; and nardilysin for acute coronary syndrome [44]. Here, we report on antibodies.