Proteomic exploration of common pathophysiological pathways in diabetes and cardiovascular disease.
Cardiometabolic disease
Cardiovascular disease
Cathepsin D
Diabetes
Galectin-4
Proteomics
Journal
ESC heart failure
ISSN: 2055-5822
Titre abrégé: ESC Heart Fail
Pays: England
ID NLM: 101669191
Informations de publication
Date de publication:
Dec 2020
Dec 2020
Historique:
revised:
07
08
2020
received:
04
05
2020
accepted:
15
09
2020
pubmed:
14
10
2020
medline:
14
10
2020
entrez:
13
10
2020
Statut:
ppublish
Résumé
The epidemiological association between diabetes and cardiovascular disease is well established, but the pathophysiological link is complex and multifactorial. We investigated seven proteins, previously linked to incident diabetes mellitus, and their association with cardiovascular disease and mortality. Plasma samples from 1713 individuals from the Swedish population-based Malmö Preventive Project (mean age 67.4 ± 6.0 years; 29.1% women) were analysed with a proximity extension assay panel. Seven proteins [scavenger receptor cysteine rich type 1 protein M130 (CD163), fatty acid-binding protein 4 (FABP4), plasminogen activator inhibitor 1 (PAI), insulin-like growth factor-binding protein 2 (IGFB2), cathepsin D (CTSD), galectin-4 (GAL4), and paraoxonase-3 (PON3)] previously shown to be associated with incident diabetes were analysed for associations with all-cause mortality (ACM), cardiovascular mortality (CVM), incident coronary events (CEs), and incident heart failure (HF). After exclusion of prevalent cases of respective outcome, proteins that met Bonferroni-corrected significance were analysed in multivariable Cox regression models. Significant associations were identified between five proteins [GAL4 (hazard ratio; 95% confidence interval: 1.17-1.41), CTSD (1.15-1.37), CD163 (1.09-1.30), IGFBP2 (1.05-1.30), and FABP4 (1.04-1.29)] and ACM and four proteins [GAL4 (1.38-1.56), CTSD (1.14-1.43), CD163 (1.09-1.36), and IGFBP2 (1.03-1.35)] with CVM. Three proteins [GAL4 (1.14-1.57), CTSD (1.12-1.50), and FABP4 (1.05-1.55)] were significantly associated with incident CE and two [GAL4 (1.03-1.54) and CTSD (1.01-1.46)] were associated with incident HF after adjusting for traditional risk factors including N-terminal pro-brain natriuretic peptide. In a general Swedish population, four proteins previously shown to be associated with diabetes were associated with ACM and CVM. Three proteins were associated with incident CE. Finally, GAL4 and CTSD displayed novel associations with incident HF and were the only proteins associated with all outcomes.
Identifiants
pubmed: 33047884
doi: 10.1002/ehf2.13036
pmc: PMC7754972
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
4151-4158Subventions
Organisme : Crafoordska Stiftelsen
Organisme : Ernhold Lundström Stiftelse
Organisme : Hjärt-Lungfonden
Organisme : Medicinska Fakulteten, Lunds Universitet (SE)
ID : ALFSKANE-432021) (ALFSKANE-436111
Organisme : Skånes universitetssjukhus
Organisme : Sydvästra Skånes Diabetesförening
Organisme : Swedish Heart-Lung Foundation
ID : 2015-0322
Organisme : Research Funds of Region Skåne
Organisme : Kock's Foundation
Organisme : Southwest Skåne's Diabetes Foundation
Organisme : Hulda and Conrad Mossfelt Foundation
Organisme : Region Skåne
Organisme : Ernhold Lundstrom's Research Foundation
Organisme : Crafoord Foundation
Organisme : Skåne University Hospital
Organisme : Medical Faculty of Lund University
ID : ALFSKANE-436111
Organisme : Medical Faculty of Lund University
ID : ALFSKANE-432021
Organisme : Wallenberg Centre for Molecular Medicine, Lund University
ID : ALFSKANE-675271
Informations de copyright
© 2020 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.
Références
Booth GL, Kapral MK, Fung K, Tu JV. Relation between age and cardiovascular disease in men and women with diabetes compared with non-diabetic people: a population-based retrospective cohort study. Lancet 2006; 368: 29-36.
Prevention. CfDCa. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States. Atlanta, Ga, USA; 2011.
Nicholls SJ, Tuzcu EM, Kalidindi S, Wolski K, Moon KW, Sipahi I, Schoenhagen P, Nissen SE. Effect of diabetes on progression of coronary atherosclerosis and arterial remodeling: a pooled analysis of 5 intravascular ultrasound trials. J Am Coll Cardiol 2008; 52: 255-262.
Parving HH, Brenner BM, McMurray JJ, de Zeeuw D, Haffner SM, Solomon SD, Chaturvedi N, Persson F, Desai AS, Nicolaides M, Richard A, Xiang Z, Brunel P, Pfeffer MA, ALTITUDE Investigators. Cardiorenal end points in a trial of aliskiren for type 2 diabetes. N Engl J Med 2012; 367: 2204-2213.
Bertoni AG, Hundley WG, Massing MW, Bonds DE, Burke GL, Goff DC Jr. Heart failure prevalence, incidence, and mortality in the elderly with diabetes. Diabetes Care 2004; 27: 699-703.
Low Wang CC, Hess CN, Hiatt WR, Goldfine AB. Clinical update: cardiovascular disease in diabetes mellitus: atherosclerotic cardiovascular disease and heart failure in type 2 diabetes mellitus-mechanisms, management, and clinical considerations. Circulation 2016; 133: 2459-2502.
Control G, Turnbull FM, Abraira C, Anderson RJ, Byington RP, Chalmers JP, Duckworth WC, Evans GW, Gerstein HC, Holman RR, Moritz TE, Neal BC. Intensive glucose control and macrovascular outcomes in type 2 diabetes. Diabetologia 2009; 52: 2288-2298.
Investigators DT, Dagenais GR, Gerstein HC, Holman R, Budaj A, Escalante A. Effects of ramipril and rosiglitazone on cardiovascular and renal outcomes in people with impaired glucose tolerance or impaired fasting glucose: results of the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) trial. Diabetes Care 2008; 31: 1007-1014.
Scirica BM, Braunwald E, Raz I, Cavender MA, Morrow DA, Jarolim P, Udell JA, Mosenzon O, Im K, Umez-Eronini AA, Pollack PS, Hirshberg B, Frederich R, Lewis BS, McGuire D, Davidson J, Steg PG, Bhatt DL, SAVOR-TIMI 53 Steering Committee and Investigators*. Heart failure, saxagliptin, and diabetes mellitus: observations from the SAVOR-TIMI 53 randomized trial. Circulation 2014; 130: 1579-1588.
Assarsson E, Lundberg M, Holmquist G, Bjorkesten J, Thorsen SB, Ekman D, Eriksson A, Dickens ER, Ohlsson S, Edfeldt G, Andersson AC. Homogenous 96-plex PEA immunoassay exhibiting high sensitivity, specificity, and excellent scalability. PLoS ONE 2014; 9: e95192.
Molvin J, Pareek M, Jujic A, Melander O, Rastam L, Lindblad U, Daka B, Leósdóttir M, Nilsson PM, Olsen MH, Magnusson M. Using a targeted proteomics chip to explore pathophysiological pathways for incident diabetes-the Malmo Preventive Project. Sci Rep 2019; 9: 272.
Leosdottir M, Willenheimer R, Plehn J, Borgquist R, Gudmundsson P, Harris TB, Launer LJ, Bjornsdottir H, Nilsson PM, Gudnason V. Myocardial structure and function by echocardiography in relation to glucometabolic status in elderly subjects from 2 population-based cohorts: a cross-sectional study. Am Heart J 2010; 159: 414-420 e4.
Moller HJ, Frikke-Schmidt R, Moestrup SK, Nordestgaard BG, Tybjaerg-Hansen A. Serum soluble CD163 predicts risk of type 2 diabetes in the general population. Clin Chem 2011; 57: 291-297.
Aristoteli LP, Moller HJ, Bailey B, Moestrup SK, Kritharides L. The monocytic lineage specific soluble CD163 is a plasma marker of coronary atherosclerosis. Atherosclerosis 2006; 184: 342-347.
Moller HJ. Soluble CD163. Scand J Clin Lab Invest 2012; 72: 1-13.
Ho JE, Lyass A, Courchesne P, Chen G, Liu C, Yin X, Hwang SJ, Massaro JM, Larson MG, Levy D. Protein biomarkers of cardiovascular disease and mortality in the community. J Am Heart Assoc 2018; 7: e008108
Hotamisligil GS, Bernlohr DA. Metabolic functions of FABPs-mechanisms and therapeutic implications. Nat Rev Endocrinol 2015; 11: 592-605.
Cao ZQ, Guo XL. The role of galectin-4 in physiology and diseases. Protein Cell 2016; 7: 314-324.
Huflejt ME, Leffler H. Galectin-4 in normal tissues and cancer. Glycoconj J 2004; 20: 247-255.
Delacour D, Gouyer V, Zanetta JP, Drobecq H, Leteurtre E, Grard G, Moreau-Hannedouche O, Maes E, Pons A, André S, Le Bivic A. Galectin-4 and sulfatides in apical membrane trafficking in enterocyte-like cells. J Cell Biol 2005; 169: 491-501.
Zhong J, Maiseyeu A, Davis SN, Rajagopalan S. DPP4 in cardiometabolic disease: recent insights from the laboratory and clinical trials of DPP4 inhibition. Circ Res 2015; 116: 1491-1504.
Drucker DJ, Nauck MA. The incretin system: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes. Lancet 2006; 368: 1696-1705.
Li L, Li S, Deng K, Liu J, Vandvik PO, Zhao P, Zhang L, Shen J, Bala MM, Sohani ZN, Wong E. Dipeptidyl peptidase-4 inhibitors and risk of heart failure in type 2 diabetes: systematic review and meta-analysis of randomised and observational studies. BMJ 2016; 352: i610.
Marso SP, Daniels GH, Brown-Frandsen K, Kristensen P, Mann JF, Nauck MA, Nissen SE, Pocock S, Poulter NR, Ravn LS, Steinberg WM, Stockner M, Zinman B, Bergenstal RM, Buse JB, LEADER Steering Committee, LEADER Trial Investigators. Liraglutide and cardiovascular outcomes in type 2 diabetes. N Engl J Med 2016; 375: 311-322.
Ljungberg J, Janiec M, Bergdahl IA, Holmgren A, Hultdin J, Johansson B, Näslund U, Siegbahn A, Fall T, Söderberg S. Proteomic biomarkers for incident aortic stenosis requiring valvular replacement. Circulation 2018; 138: 590-599.
Choi B, Lee S, Kim SM, Lee EJ, Lee SR, Kim DH, Jang JY, Kang SW, Lee KU, Chang EJ, Song JK. Dipeptidyl peptidase-4 induces aortic valve calcification by inhibiting insulin-like growth factor-1 signaling in valvular interstitial cells. Circulation 2017; 135: 1935-1950.
Goncalves I, Hultman K, Duner P, Edsfeldt A, Hedblad B, Fredrikson GN, Björkbacka H, Nilsson J, Bengtsson E. High levels of cathepsin D and cystatin B are associated with increased risk of coronary events. Open Heart 2016; 3: e000353.
Benes P, Vetvicka V, Fusek M. Cathepsin D-many functions of one aspartic protease. Crit Rev Oncol Hematol 2008; 68: 12-28.
Hakala JK, Oksjoki R, Laine P, Du H, Grabowski GA, Kovanen PT, Pentikäinen MO. Lysosomal enzymes are released from cultured human macrophages, hydrolyze LDL in vitro, and are present extracellularly in human atherosclerotic lesions. Arterioscler Thromb Vasc Biol 2003; 23: 1430-1436.
Mallat Z, Tedgui A. Apoptosis in the vasculature: mechanisms and functional importance. Br J Pharmacol 2000; 130: 947-962.
Cubedo J, Padro T, Garcia-Arguinzonis M, Vilahur G, Minambres I, Pou JM, Ybarra J, Badimon L. A novel truncated form of apolipoprotein A-I transported by dense LDL is increased in diabetic patients. J Lipid Res 2015; 56: 1762-1773.
Vivanco F, Martin-Ventura JL, Duran MC, Barderas MG, Blanco-Colio L, Darde VM, Mas S, Meilhac O, Michel JB, Tuñón J, Egido J. Quest for novel cardiovascular biomarkers by proteomic analysis. J Proteome Res 2005; 4: 1181-1191.
Kundi H, Balun A, Cicekcioglu H, Cetin M, Kiziltunc E, Topcuoglu C, Fevzi Kilinckaya M, Ornek E. Admission value of serum cathepsin D level can be useful for predicting in-hospital mortality in patients with NSTEMI. Acta Cardiol Sin 2017; 33: 393-400.
Yamac AH, Sevgili E, Kucukbuzcu S, Nasifov M, Ismailoglu Z, Kilic E, Ercan C, Jafarov P, Uyarel H, Bacaksiz A. Role of cathepsin D activation in major adverse cardiovascular events and new-onset heart failure after STEMI. Herz 2015; 40: 912-920.