The Neoepitopes on Methylglyoxal- (MG-) Glycated Fibrinogen Generate Autoimmune Response: Its Role in Diabetes, Atherosclerosis, and Diabetic Atherosclerosis Subjects
Objectives. In diabetes mellitus, hyperglycemia-mediated nonenzymatic glycosylation of fibrinogen protein plays a crucial role in the pathogenesis of micro- and macrovascular complications especially atherosclerosis via the generation of advanced glycation end products (AGEs). Methylglyoxal (MG) ind...
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| Published in | Oxidative medicine and cellular longevity Vol. 2021; no. 1; p. 6621568 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Hindawi
2021
John Wiley & Sons, Inc |
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| Abstract | Objectives. In diabetes mellitus, hyperglycemia-mediated nonenzymatic glycosylation of fibrinogen protein plays a crucial role in the pathogenesis of micro- and macrovascular complications especially atherosclerosis via the generation of advanced glycation end products (AGEs). Methylglyoxal (MG) induces glycation of fibrinogen, resulting in structural alterations that lead to autoimmune response via the generation of neoepitopes on protein molecules. The present study was designed to probe the prevalence of autoantibodies against MG-glycated fibrinogen (MG-Fib) in type 2 diabetes mellitus (T2DM), atherosclerosis (ATH), and diabetic atherosclerosis (T2DM-ATH) patients. Design and Methods. The binding affinity of autoantibodies in patients’ sera (T2DM, n=100; ATH, n=100; and T2DM-ATH, n=100) and isolated immunoglobulin G (IgG) against native fibrinogen (N-Fib) and MG-Fib to healthy subjects (HS, n=50) was accessed by direct binding ELISA. The results of direct binding were further validated by competitive/inhibition ELISA. Moreover, AGE detection, ketoamines, protein carbonyls, hydroxymethylfurfural (HMF), thiobarbituric acid reactive substances (TBARS), and carboxymethyllysine (CML) concentrations in patients’ sera were also determined. Furthermore, free lysine and free arginine residues were also estimated. Results. The high binding affinity was observed in 54% of T2DM, 33% of ATH, and 65% of T2DM-ATH patients’ samples with respect to healthy subjects against MG-Fib antigen in comparison to N-Fib (p<0.05 to p<0.0001). HS sera showed nonsignificant binding (p>0.05) with N-Fib and MG-Fib. Other biochemical parameters were also found to be significant (p<0.05) in the patient groups with respect to the HS group. Conclusions. These findings in the future might pave a way to authenticate fibrinogen as a biomarker for the early detection of diabetes-associated micro- and macrovascular complications. |
|---|---|
| AbstractList | Objectives
. In diabetes mellitus, hyperglycemia‐mediated nonenzymatic glycosylation of fibrinogen protein plays a crucial role in the pathogenesis of micro‐ and macrovascular complications especially atherosclerosis via the generation of advanced glycation end products (AGEs). Methylglyoxal (MG) induces glycation of fibrinogen, resulting in structural alterations that lead to autoimmune response via the generation of neoepitopes on protein molecules. The present study was designed to probe the prevalence of autoantibodies against MG‐glycated fibrinogen (MG‐Fib) in type 2 diabetes mellitus (T2DM), atherosclerosis (ATH), and diabetic atherosclerosis (T2DM‐ATH) patients.
Design and Methods
. The binding affinity of autoantibodies in patients’ sera (T2DM,
n
= 100; ATH,
n
= 100; and T2DM‐ATH,
n
= 100) and isolated immunoglobulin G (IgG) against native fibrinogen (N‐Fib) and MG‐Fib to healthy subjects (HS,
n
= 50) was accessed by direct binding ELISA. The results of direct binding were further validated by competitive/inhibition ELISA. Moreover, AGE detection, ketoamines, protein carbonyls, hydroxymethylfurfural (HMF), thiobarbituric acid reactive substances (TBARS), and carboxymethyllysine (CML) concentrations in patients’ sera were also determined. Furthermore, free lysine and free arginine residues were also estimated.
Results
. The high binding affinity was observed in 54% of T2DM, 33% of ATH, and 65% of T2DM‐ATH patients’ samples with respect to healthy subjects against MG‐Fib antigen in comparison to N‐Fib (
p
< 0.05 to
p
< 0.0001). HS sera showed nonsignificant binding (
p
> 0.05) with N‐Fib and MG‐Fib. Other biochemical parameters were also found to be significant (
p
< 0.05) in the patient groups with respect to the HS group.
Conclusions
. These findings in the future might pave a way to authenticate fibrinogen as a biomarker for the early detection of diabetes‐associated micro‐ and macrovascular complications. In diabetes mellitus, hyperglycemia-mediated nonenzymatic glycosylation of fibrinogen protein plays a crucial role in the pathogenesis of micro- and macrovascular complications especially atherosclerosis via the generation of advanced glycation end products (AGEs). Methylglyoxal (MG) induces glycation of fibrinogen, resulting in structural alterations that lead to autoimmune response via the generation of neoepitopes on protein molecules. The present study was designed to probe the prevalence of autoantibodies against MG-glycated fibrinogen (MG-Fib) in type 2 diabetes mellitus (T2DM), atherosclerosis (ATH), and diabetic atherosclerosis (T2DM-ATH) patients. . The binding affinity of autoantibodies in patients' sera (T2DM, = 100; ATH, = 100; and T2DM-ATH, = 100) and isolated immunoglobulin G (IgG) against native fibrinogen (N-Fib) and MG-Fib to healthy subjects (HS, = 50) was accessed by direct binding ELISA. The results of direct binding were further validated by competitive/inhibition ELISA. Moreover, AGE detection, ketoamines, protein carbonyls, hydroxymethylfurfural (HMF), thiobarbituric acid reactive substances (TBARS), and carboxymethyllysine (CML) concentrations in patients' sera were also determined. Furthermore, free lysine and free arginine residues were also estimated. The high binding affinity was observed in 54% of T2DM, 33% of ATH, and 65% of T2DM-ATH patients' samples with respect to healthy subjects against MG-Fib antigen in comparison to N-Fib ( < 0.05 to < 0.0001). HS sera showed nonsignificant binding ( > 0.05) with N-Fib and MG-Fib. Other biochemical parameters were also found to be significant ( < 0.05) in the patient groups with respect to the HS group. These findings in the future might pave a way to authenticate fibrinogen as a biomarker for the early detection of diabetes-associated micro- and macrovascular complications. In diabetes mellitus, hyperglycemia-mediated nonenzymatic glycosylation of fibrinogen protein plays a crucial role in the pathogenesis of micro- and macrovascular complications especially atherosclerosis via the generation of advanced glycation end products (AGEs). Methylglyoxal (MG) induces glycation of fibrinogen, resulting in structural alterations that lead to autoimmune response via the generation of neoepitopes on protein molecules. The present study was designed to probe the prevalence of autoantibodies against MG-glycated fibrinogen (MG-Fib) in type 2 diabetes mellitus (T2DM), atherosclerosis (ATH), and diabetic atherosclerosis (T2DM-ATH) patients. Design and Methods. The binding affinity of autoantibodies in patients' sera (T2DM, n = 100; ATH, n = 100; and T2DM-ATH, n = 100) and isolated immunoglobulin G (IgG) against native fibrinogen (N-Fib) and MG-Fib to healthy subjects (HS, n = 50) was accessed by direct binding ELISA. The results of direct binding were further validated by competitive/inhibition ELISA. Moreover, AGE detection, ketoamines, protein carbonyls, hydroxymethylfurfural (HMF), thiobarbituric acid reactive substances (TBARS), and carboxymethyllysine (CML) concentrations in patients' sera were also determined. Furthermore, free lysine and free arginine residues were also estimated.OBJECTIVESIn diabetes mellitus, hyperglycemia-mediated nonenzymatic glycosylation of fibrinogen protein plays a crucial role in the pathogenesis of micro- and macrovascular complications especially atherosclerosis via the generation of advanced glycation end products (AGEs). Methylglyoxal (MG) induces glycation of fibrinogen, resulting in structural alterations that lead to autoimmune response via the generation of neoepitopes on protein molecules. The present study was designed to probe the prevalence of autoantibodies against MG-glycated fibrinogen (MG-Fib) in type 2 diabetes mellitus (T2DM), atherosclerosis (ATH), and diabetic atherosclerosis (T2DM-ATH) patients. Design and Methods. The binding affinity of autoantibodies in patients' sera (T2DM, n = 100; ATH, n = 100; and T2DM-ATH, n = 100) and isolated immunoglobulin G (IgG) against native fibrinogen (N-Fib) and MG-Fib to healthy subjects (HS, n = 50) was accessed by direct binding ELISA. The results of direct binding were further validated by competitive/inhibition ELISA. Moreover, AGE detection, ketoamines, protein carbonyls, hydroxymethylfurfural (HMF), thiobarbituric acid reactive substances (TBARS), and carboxymethyllysine (CML) concentrations in patients' sera were also determined. Furthermore, free lysine and free arginine residues were also estimated.The high binding affinity was observed in 54% of T2DM, 33% of ATH, and 65% of T2DM-ATH patients' samples with respect to healthy subjects against MG-Fib antigen in comparison to N-Fib (p < 0.05 to p < 0.0001). HS sera showed nonsignificant binding (p > 0.05) with N-Fib and MG-Fib. Other biochemical parameters were also found to be significant (p < 0.05) in the patient groups with respect to the HS group.RESULTSThe high binding affinity was observed in 54% of T2DM, 33% of ATH, and 65% of T2DM-ATH patients' samples with respect to healthy subjects against MG-Fib antigen in comparison to N-Fib (p < 0.05 to p < 0.0001). HS sera showed nonsignificant binding (p > 0.05) with N-Fib and MG-Fib. Other biochemical parameters were also found to be significant (p < 0.05) in the patient groups with respect to the HS group.These findings in the future might pave a way to authenticate fibrinogen as a biomarker for the early detection of diabetes-associated micro- and macrovascular complications.CONCLUSIONSThese findings in the future might pave a way to authenticate fibrinogen as a biomarker for the early detection of diabetes-associated micro- and macrovascular complications. Objectives. In diabetes mellitus, hyperglycemia-mediated nonenzymatic glycosylation of fibrinogen protein plays a crucial role in the pathogenesis of micro- and macrovascular complications especially atherosclerosis via the generation of advanced glycation end products (AGEs). Methylglyoxal (MG) induces glycation of fibrinogen, resulting in structural alterations that lead to autoimmune response via the generation of neoepitopes on protein molecules. The present study was designed to probe the prevalence of autoantibodies against MG-glycated fibrinogen (MG-Fib) in type 2 diabetes mellitus (T2DM), atherosclerosis (ATH), and diabetic atherosclerosis (T2DM-ATH) patients. Design and Methods. The binding affinity of autoantibodies in patients’ sera (T2DM, n=100; ATH, n=100; and T2DM-ATH, n=100) and isolated immunoglobulin G (IgG) against native fibrinogen (N-Fib) and MG-Fib to healthy subjects (HS, n=50) was accessed by direct binding ELISA. The results of direct binding were further validated by competitive/inhibition ELISA. Moreover, AGE detection, ketoamines, protein carbonyls, hydroxymethylfurfural (HMF), thiobarbituric acid reactive substances (TBARS), and carboxymethyllysine (CML) concentrations in patients’ sera were also determined. Furthermore, free lysine and free arginine residues were also estimated. Results. The high binding affinity was observed in 54% of T2DM, 33% of ATH, and 65% of T2DM-ATH patients’ samples with respect to healthy subjects against MG-Fib antigen in comparison to N-Fib (p<0.05 to p<0.0001). HS sera showed nonsignificant binding (p>0.05) with N-Fib and MG-Fib. Other biochemical parameters were also found to be significant (p<0.05) in the patient groups with respect to the HS group. Conclusions. These findings in the future might pave a way to authenticate fibrinogen as a biomarker for the early detection of diabetes-associated micro- and macrovascular complications. |
| Author | Faisal, Mohammad Akhter, Firoz Rehman, Shahnawaz Ahmad, Saheem Alatar, Abdulrahman A. Hu, Bo Song, Jiantao |
| AuthorAffiliation | 3 Department of Botany & Microbiology, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia 1 Department of Biochemistry, Sir Syed Faculty of Science, Mohammad Ali Jauhar University, Rampur, U.P., India 2 Department of Emergency, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China 4 Department of Biomedical Engineering, Stony Brook University, New York, USA 5 Department of Medical Laboratory Sciences, College of Applied Medical Sciences, University of Hail, 2440, Saudi Arabia |
| AuthorAffiliation_xml | – name: 2 Department of Emergency, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China – name: 4 Department of Biomedical Engineering, Stony Brook University, New York, USA – name: 5 Department of Medical Laboratory Sciences, College of Applied Medical Sciences, University of Hail, 2440, Saudi Arabia – name: 1 Department of Biochemistry, Sir Syed Faculty of Science, Mohammad Ali Jauhar University, Rampur, U.P., India – name: 3 Department of Botany & Microbiology, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34970417$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_abb_2024_109911 crossref_primary_10_1002_cbf_3722 crossref_primary_10_1016_j_cca_2023_117684 crossref_primary_10_3389_fendo_2024_1371682 crossref_primary_10_1016_j_ijbiomac_2022_02_093 crossref_primary_10_1186_s40001_024_01739_1 |
| Cites_doi | 10.2174/1570161115666170327162639 10.1007/s10741-013-9374-y 10.1177/000456329102800613 10.1016/0003-2697(79)90738-3 10.1042/bj2910529 10.3906/biy-1501-71 10.1016/j.diabres.2018.04.025 10.1002/jcb.26146 10.1007/s00059-004-2607-z 10.1182/blood-2006-08-040956 10.1016/0014-5793(88)80066-8 10.1002/jcla.22039 10.5507/bp.2011.013 10.2337/diabetes.54.6.1615 10.1016/j.ijbiomac.2021.01.197 10.1016/j.thromres.2006.10.016 10.1016/S0891-5849(02)00780-3 10.1016/j.diabres.2004.09.004 10.1042/BST20140009 10.1002/jcb.27170 10.1016/j.abb.2018.02.019 10.3109/08916934.2014.941059 10.1007/s00125-005-1742-2 10.1042/BCJ20160503C 10.1016/0003-2697(69)90032-3 10.1016/j.ijbiomac.2018.04.016 10.3389/fchem.2017.00039 10.1007/s12013-014-9991-7 10.1155/2011/718694 10.1016/0002-9149(93)90142-Y 10.1016/j.jdiacomp.2015.12.018 10.1016/j.lfs.2016.02.013 10.1016/j.ijbiomac.2014.10.034 10.1093/glycob/cwu057 10.2337/diab.32.7.680 10.1016/j.metabol.2009.09.010 10.1093/clinchem/44.3.522 10.1021/ac0514220 10.1016/j.semcancer.2017.10.005 10.1155/2014/417842 10.3390/ijms18050984 10.1007/s11010-019-03550-7 10.1155/2017/1209676 10.1152/ajpendo.00535.2001 10.1007/s12013-015-0713-6 10.1016/j.bbrc.2011.03.064 10.1006/bbrc.1997.7718 10.2169/internalmedicine.38.309 10.1093/oxfordjournals.jbchem.a022062 10.1371/journal.pone.0053205 10.1016/0009-8981(83)90078-5 10.1016/S0076-6879(94)33040-9 10.1016/j.cbi.2014.06.012 10.1016/j.ijbiomac.2013.08.037 10.1210/er.2018-00141 10.1042/bj20030763 10.1016/j.biopha.2017.10.122 10.1042/BST20140018 10.1007/s11010-010-0541-3 10.1042/bj3440109 10.1007/s12013-011-9335-9 10.1016/j.semcancer.2017.07.001 10.1016/j.jcte.2014.05.002 10.2741/s474 10.1371/journal.pone.0191014 10.1016/S0009-8981(03)00003-2 10.1093/glycob/cwz012 10.3109/10715768809066899 10.1016/j.cellimm.2020.104062 10.1152/ajpendo.00274.2003 10.1002/9783527633500 |
| ContentType | Journal Article |
| Copyright | Copyright © 2021 Shahnawaz Rehman et al. Copyright © 2021 Shahnawaz Rehman et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0 Copyright © 2021 Shahnawaz Rehman et al. 2021 |
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| References | e_1_2_11_70_2 e_1_2_11_30_2 e_1_2_11_55_2 e_1_2_11_76_2 e_1_2_11_57_2 e_1_2_11_13_2 La Cote A. L. C. (e_1_2_11_27_2) 2011 e_1_2_11_34_2 e_1_2_11_51_2 e_1_2_11_72_2 e_1_2_11_11_2 e_1_2_11_32_2 e_1_2_11_53_2 e_1_2_11_74_2 e_1_2_11_6_2 e_1_2_11_4_2 e_1_2_11_25_2 e_1_2_11_2_2 e_1_2_11_48_2 e_1_2_11_69_2 e_1_2_11_29_2 e_1_2_11_60_2 Hatton M. W. (e_1_2_11_24_2) 1993; 121 e_1_2_11_20_2 e_1_2_11_43_2 e_1_2_11_66_2 e_1_2_11_45_2 e_1_2_11_68_2 e_1_2_11_62_2 e_1_2_11_8_2 e_1_2_11_22_2 e_1_2_11_41_2 e_1_2_11_64_2 e_1_2_11_17_2 e_1_2_11_15_2 e_1_2_11_36_2 Rehman S. (e_1_2_11_38_2) 2019; 20 e_1_2_11_59_2 e_1_2_11_19_2 e_1_2_11_71_2 e_1_2_11_31_2 e_1_2_11_54_2 e_1_2_11_56_2 e_1_2_11_35_2 e_1_2_11_50_2 e_1_2_11_12_2 e_1_2_11_33_2 e_1_2_11_52_2 e_1_2_11_75_2 e_1_2_11_10_2 e_1_2_11_28_2 e_1_2_11_5_2 e_1_2_11_26_2 e_1_2_11_3_2 e_1_2_11_47_2 e_1_2_11_1_2 e_1_2_11_49_2 Ahmad R. (e_1_2_11_73_2) 2008; 22 e_1_2_11_44_2 e_1_2_11_65_2 e_1_2_11_46_2 e_1_2_11_67_2 e_1_2_11_9_2 e_1_2_11_23_2 e_1_2_11_40_2 e_1_2_11_61_2 e_1_2_11_7_2 e_1_2_11_21_2 e_1_2_11_42_2 e_1_2_11_63_2 e_1_2_11_16_2 e_1_2_11_14_2 e_1_2_11_58_2 e_1_2_11_37_2 e_1_2_11_18_2 e_1_2_11_39_2 |
| References_xml | – ident: e_1_2_11_4_2 doi: 10.2174/1570161115666170327162639 – ident: e_1_2_11_2_2 doi: 10.1007/s10741-013-9374-y – ident: e_1_2_11_29_2 doi: 10.1177/000456329102800613 – ident: e_1_2_11_56_2 doi: 10.1016/0003-2697(79)90738-3 – ident: e_1_2_11_67_2 doi: 10.1042/bj2910529 – ident: e_1_2_11_3_2 doi: 10.3906/biy-1501-71 – ident: e_1_2_11_20_2 doi: 10.1016/j.diabres.2018.04.025 – start-page: 75 volume-title: Advances in protein chemistry and structural biology year: 2011 ident: e_1_2_11_27_2 – ident: e_1_2_11_37_2 doi: 10.1002/jcb.26146 – volume: 121 start-page: 588 year: 1993 ident: e_1_2_11_24_2 article-title: Catabolism of unglycated and naturally glycated forms of rabbit fibrinogen: their interaction with the healthy and deendothelialized aorta wall in normal and diabetic rabbits publication-title: The Journal of Laboratory and Clinical Medicine – ident: e_1_2_11_25_2 doi: 10.1007/s00059-004-2607-z – ident: e_1_2_11_19_2 doi: 10.1182/blood-2006-08-040956 – ident: e_1_2_11_62_2 doi: 10.1016/0014-5793(88)80066-8 – ident: e_1_2_11_42_2 doi: 10.1002/jcla.22039 – ident: e_1_2_11_72_2 doi: 10.5507/bp.2011.013 – ident: e_1_2_11_1_2 doi: 10.2337/diabetes.54.6.1615 – ident: e_1_2_11_76_2 doi: 10.1016/j.ijbiomac.2021.01.197 – ident: e_1_2_11_21_2 doi: 10.1016/j.thromres.2006.10.016 – ident: e_1_2_11_68_2 doi: 10.1016/S0891-5849(02)00780-3 – ident: e_1_2_11_75_2 doi: 10.1016/j.diabres.2004.09.004 – ident: e_1_2_11_13_2 doi: 10.1042/BST20140009 – ident: e_1_2_11_60_2 doi: 10.1002/jcb.27170 – ident: e_1_2_11_65_2 doi: 10.1016/j.abb.2018.02.019 – ident: e_1_2_11_46_2 doi: 10.3109/08916934.2014.941059 – ident: e_1_2_11_26_2 doi: 10.1007/s00125-005-1742-2 – ident: e_1_2_11_7_2 doi: 10.1042/BCJ20160503C – ident: e_1_2_11_57_2 doi: 10.1016/0003-2697(69)90032-3 – ident: e_1_2_11_59_2 doi: 10.1016/j.ijbiomac.2018.04.016 – ident: e_1_2_11_32_2 – ident: e_1_2_11_15_2 doi: 10.3389/fchem.2017.00039 – ident: e_1_2_11_50_2 doi: 10.1007/s12013-014-9991-7 – ident: e_1_2_11_58_2 doi: 10.1155/2011/718694 – ident: e_1_2_11_16_2 doi: 10.1016/0002-9149(93)90142-Y – ident: e_1_2_11_22_2 doi: 10.1016/j.jdiacomp.2015.12.018 – ident: e_1_2_11_41_2 doi: 10.1016/j.lfs.2016.02.013 – ident: e_1_2_11_40_2 doi: 10.1016/j.ijbiomac.2014.10.034 – ident: e_1_2_11_17_2 doi: 10.1093/glycob/cwu057 – volume: 20 start-page: 1 year: 2019 ident: e_1_2_11_38_2 article-title: Physico-chemical changes induced in serum proteins, immunoglobulin-G and fibrinogen by reactive carbonyl species, methylglyoxal publication-title: Current Protein & Peptide Science – ident: e_1_2_11_30_2 doi: 10.2337/diab.32.7.680 – ident: e_1_2_11_51_2 doi: 10.1016/j.metabol.2009.09.010 – ident: e_1_2_11_63_2 doi: 10.1093/clinchem/44.3.522 – ident: e_1_2_11_70_2 doi: 10.1021/ac0514220 – volume: 22 start-page: 525 year: 2008 ident: e_1_2_11_73_2 article-title: Malondialdehyde and protein carbonyl as biomarkers for oxidative stress and disease progression in patients with chronic myeloid leukemia publication-title: in vivo – ident: e_1_2_11_6_2 doi: 10.1016/j.semcancer.2017.10.005 – ident: e_1_2_11_9_2 doi: 10.1155/2014/417842 – ident: e_1_2_11_10_2 doi: 10.3390/ijms18050984 – ident: e_1_2_11_8_2 doi: 10.1007/s11010-019-03550-7 – ident: e_1_2_11_28_2 doi: 10.1155/2017/1209676 – ident: e_1_2_11_34_2 doi: 10.1152/ajpendo.00535.2001 – ident: e_1_2_11_52_2 doi: 10.1007/s12013-015-0713-6 – ident: e_1_2_11_45_2 doi: 10.1016/j.bbrc.2011.03.064 – ident: e_1_2_11_31_2 doi: 10.1006/bbrc.1997.7718 – ident: e_1_2_11_71_2 doi: 10.2169/internalmedicine.38.309 – ident: e_1_2_11_35_2 doi: 10.1093/oxfordjournals.jbchem.a022062 – ident: e_1_2_11_48_2 doi: 10.1371/journal.pone.0053205 – ident: e_1_2_11_49_2 doi: 10.1016/0009-8981(83)90078-5 – ident: e_1_2_11_53_2 doi: 10.1016/S0076-6879(94)33040-9 – ident: e_1_2_11_47_2 doi: 10.1016/j.cbi.2014.06.012 – ident: e_1_2_11_55_2 doi: 10.1016/j.ijbiomac.2013.08.037 – ident: e_1_2_11_23_2 doi: 10.1210/er.2018-00141 – ident: e_1_2_11_74_2 doi: 10.1042/bj20030763 – ident: e_1_2_11_36_2 doi: 10.1016/j.biopha.2017.10.122 – ident: e_1_2_11_14_2 doi: 10.1042/BST20140018 – ident: e_1_2_11_5_2 doi: 10.1007/s11010-010-0541-3 – ident: e_1_2_11_11_2 doi: 10.1042/bj3440109 – ident: e_1_2_11_64_2 doi: 10.1007/s12013-011-9335-9 – ident: e_1_2_11_18_2 doi: 10.1016/j.semcancer.2017.07.001 – ident: e_1_2_11_39_2 doi: 10.1016/j.jcte.2014.05.002 – ident: e_1_2_11_12_2 doi: 10.2741/s474 – ident: e_1_2_11_54_2 doi: 10.1371/journal.pone.0191014 – ident: e_1_2_11_69_2 doi: 10.1016/S0009-8981(03)00003-2 – ident: e_1_2_11_43_2 doi: 10.1093/glycob/cwz012 – ident: e_1_2_11_61_2 doi: 10.3109/10715768809066899 – ident: e_1_2_11_44_2 doi: 10.1016/j.cellimm.2020.104062 – ident: e_1_2_11_33_2 doi: 10.1152/ajpendo.00274.2003 – ident: e_1_2_11_66_2 doi: 10.1002/9783527633500 |
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| Snippet | Objectives. In diabetes mellitus, hyperglycemia-mediated nonenzymatic glycosylation of fibrinogen protein plays a crucial role in the pathogenesis of micro-... Objectives . In diabetes mellitus, hyperglycemia‐mediated nonenzymatic glycosylation of fibrinogen protein plays a crucial role in the pathogenesis of micro‐... In diabetes mellitus, hyperglycemia-mediated nonenzymatic glycosylation of fibrinogen protein plays a crucial role in the pathogenesis of micro- and... |
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| SubjectTerms | Adult Atherosclerosis Atherosclerosis - physiopathology Diabetes Diabetes Mellitus, Type 2 - physiopathology Female Fibrinogen - metabolism Glucose Humans Hyperglycemia Male Middle Aged Oxidative stress Peptides Proteins Pyruvaldehyde - metabolism Sodium |
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| Title | The Neoepitopes on Methylglyoxal- (MG-) Glycated Fibrinogen Generate Autoimmune Response: Its Role in Diabetes, Atherosclerosis, and Diabetic Atherosclerosis Subjects |
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