1. Olefsky, JM, Glass, CK. Macrophages, inflammation, and insulin resistance. Annu Rev Physiol 2010; 72: 219–246.
Google Scholar | Crossref | Medline | ISI2. Gregor, MF, Hotamisligil, GS. Inflammatory mechanisms in obesity. Annu Rev Immunol 2011; 29: 415–445.
Google Scholar | Crossref | Medline | ISI3. Wiedow, O, Meyer-Hoffert, U. Neutrophil serine proteases: potential key regulators of cell signalling during inflammation. J Intern Med 2005; 257: 319–328.
Google Scholar | Crossref | Medline | ISI4. Meyer-Hoffert, U, Wiedow, O. Neutrophil serine proteases: mediators of innate immune responses. Curr Opin Hematol 2011; 18: 19–24.
Google Scholar | Crossref | Medline5. Kessenbrock, K, Fröhlich, L, Sixt, M, et al. Proteinase 3 and neutrophil elastase enhance inflammation in mice by inactivating anti-inflammatory progranulin. J Clin Invest 2008; 118: 2438–2447.
Google Scholar | Medline6. Preston, GA, Zarella, CS, Pendergraft, WF, et al. Novel effects of neutrophil-derived proteinase 3 and elastase on the vascular endothelium involve in vivo cleavage of NF-kappaB and proapoptotic changes in JNK, ERK, and p38 MAPK signaling pathways. J Am Soc Nephrol 2002; 13: 2840–2849.
Google Scholar | Crossref | Medline | ISI7. Talukdar, S, Oh, DY, Bandyopadhyay, G, et al. Neutrophils mediate insulin resistance in mice fed a high-fat diet through secreted elastase. Nat Med 2012; 18: 1407–1412.
Google Scholar | Crossref | Medline | ISI8. Mansuy-Aubert, V, Zhou, QL, Xie, X, et al. Imbalance between neutrophil elastase and its inhibitor α1-antitrypsin in obesity alters insulin sensitivity, inflammation, and energy expenditure. Cell Metab 2013; 17: 534–548.
Google Scholar | Crossref | Medline | ISI9. Dollery, CM, Owen, CA, Sukhova, GK, et al. Neutrophil elastase in human atherosclerotic plaques: production by macrophages. Circulation 2003; 107: 2829–2836.
Google Scholar | Crossref | Medline | ISI10. Alfaidi, M, Wilson, H, Daigneault, M, et al. Neutrophil elastase promotes interleukin-1β secretion from human coronary endothelium. J Biol Chem 2015; 290: 24067–24078.
Google Scholar | Crossref | Medline | ISI11. Bae, S, Choi, J, Hong, J, et al. Neutrophil proteinase 3 induces diabetes in a mouse model of glucose tolerance. Endocr Res 2012; 37: 35–45.
Google Scholar | Crossref | Medline12. Mirea, AM, Toonen, EJM, Van Den Munckhof, I, et al. Increased proteinase 3 and neutrophil elastase plasma concentrations are associated with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes. Mol Med 2019; 25: 16.
Google Scholar | Crossref | Medline13. Wang, Y, Xiao, Y, Zhong, L, et al. Increased neutrophil elastase and proteinase 3 and augmented NETosis are closely associated with β-cell autoimmunity in patients with type 1 diabetes. Diabetes 2014; 63: 4239–4248.
Google Scholar | Crossref | Medline14. Ng, LL, Khan, SQ, Narayan, H, et al. Proteinase 3 and prognosis of patients with acute myocardial infarction. Clin Sci (Lond) 2011; 120: 231–238.
Google Scholar | Crossref | Medline15. Fruchart, JC. Peroxisome proliferator-activated receptor-alpha (PPARalpha): at the crossroads of obesity, diabetes and cardiovascular disease. Atherosclerosis 2009; 205: 1–8.
Google Scholar | Crossref | Medline | ISI16. FIELD Study Investigators . The need for a large-scale trial of fibrate therapy in diabetes: the rationale and design of the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study. [ISRCTN64783481]. Cardiovasc Diabetol 2004; 3: 9.
Google Scholar | Crossref | Medline17. Keech, A, Simes, RJ, Barter, P, et al. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 2005; 366: 1849–1861.
Google Scholar | Crossref | Medline | ISI18. Keech, AC, Mitchell, P, Summanen, PA, et al. Effect of fenofibrate on the need for laser treatment for diabetic retinopathy (FIELD study): a randomized controlled trial. Lancet 2007; 370: 1687–1697.
Google Scholar | Crossref | Medline | ISI19. Rajamani, K, Colman, PG, Li, LP, et al. Effect of fenofibrate on amputation events in people with type 2 diabetes mellitus (FIELD study): a prespecified analysis of a randomised controlled trial. Lancet 2009; 373: 1780–1788.
Google Scholar | Crossref | Medline | ISI20. Ting, RD, Keech, AC, Drury, PL, et al.; FIELD Study Investigators. Benefits and safety of long-term fenofibrate therapy in people with type 2 diabetes and renal impairment: the FIELD Study. Diabetes Care 2012; 35: 218–225.
Google Scholar | Crossref | Medline21. Burgess, DC, Hunt, D, Li, L, et al. Incidence and predictors of silent myocardial infarction in type 2 diabetes and the effect of fenofibrate: an analysis from the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study. Eur Heart J 2010; 31: 92–99.
Google Scholar | Crossref | Medline | ISI22. Ong, KL, Rye, KA, O’Connell, R, et al. Long-term fenofibrate therapy increases fibroblast growth factor 21 and retinol-binding protein 4 in subjects with type 2 diabetes. J Clin Endocrinol Metab 2012; 97: 4701–4708.
Google Scholar | Crossref | Medline23. Scott, R, Best, J, Forder, P, et al. Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study: baseline characteristics and short-term effects of fenofibrate [ISRCTN64783481]. Cardiovasc Diabetol 2005; 4: 13.
Google Scholar | Crossref | Medline24. Taskinen, MR, Sullivan, DR, Ehnholm, C, et al. Relationships of HDL cholesterol, ApoA-I, and ApoA-II with homocysteine and creatinine in patients with type 2 diabetes treated with fenofibrate. Arterioscler Thromb Vasc Biol 2009; 29: 950–955.
Google Scholar | Crossref | Medline25. Levey, AS, Stevens, LA, Schmid, CH, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med 2009; 150: 604–612.
Google Scholar | Crossref | Medline | ISI26. Wallace, TM, Levy, JC, Matthews, DR. Use and abuse of HOMA modeling. Diabetes Care 2004; 27: 1487–1495.
Google Scholar | Crossref | Medline | ISI27. Herrmann, M, Sullivan, DR, Veillard, AS, et al. Serum 25-hydroxyvitamin D: a predictor of macrovascular and microvascular complications in patients with type 2 diabetes. Diabetes Care 2015; 38: 521–528.
Google Scholar | Crossref | Medline | ISI28. Ong, KL, Januszewski, AS, O’Connell, R, et al. The relationship of fibroblast growth factor 21 with cardiovascular outcome events in the Fenofibrate Intervention and Event Lowering in Diabetes study. Diabetologia 2015; 58: 464–473.
Google Scholar | Crossref | Medline29. Ong, KL, Januszewski, AS, O’Connell, R, et al. Relationship of fibroblast growth factor 21 with baseline and new on-study microvascular disease in the Fenofibrate Intervention and Event Lowering in Diabetes study. Diabetologia 2015; 58: 2035–2044.
Google Scholar | Crossref | Medline30. Dali-Youcef, N, Mecili, M, Ricci, R, et al. Metabolic inflammation: connecting obesity and insulin resistance. Ann Med 2013; 45: 242–253.
Google Scholar | Crossref | Medline31. Fu, Y, Wang, X, Kong, W. Hyperhomocysteinaemia and vascular injury: advances in mechanisms and drug targets. Br J Pharmacol 2018; 175: 1173–1189.
Google Scholar | Crossref | Medline32. Ridker, PM, Everett, BM, Thuren, T, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med 2017; 377: 1119–1131.
Google Scholar | Crossref | Medline | ISI33. Pendergraft, WF, Rudolph, EH, Falk, RJ, et al. Proteinase 3 sidesteps caspases and cleaves p21(Waf1/Cip1/Sdi1) to induce endothelial cell apoptosis. Kidney Int 2004; 65: 75–84.
Google Scholar | Crossref | Medline34. Pham, CT. Neutrophil serine proteases fine-tune the inflammatory response. Int J Biochem Cell Biol 2008; 40: 1317–1333.
Google Scholar | Crossref | Medline | ISI35. Korkmaz, B, Horwitz, MS, Jenne, DE, et al. Neutrophil elastase, proteinase 3, and cathepsin G as therapeutic targets in human diseases. Pharmacol Rev 2010; 62: 726–759.
Google Scholar | Crossref | Medline | ISI36. Jerke, U, Hernandez, DP, Beaudette, P, et al. Neutrophil serine proteases exert proteolytic activity on endothelial cells. Kidney Int 2015; 88: 764–775.
Google Scholar | Crossref | Medline37. Johnson, RJ, Couser, WG, Alpers, CE, et al. The human neutrophil serine proteinases, elastase and cathepsin G, can mediate glomerular injury in vivo. J Exp Med 1988; 168: 1169–1174.
Google Scholar | Crossref | Medline38. Zager, RA, Johnson, AC, Frostad, KB. Rapid renal alpha-1 antitrypsin gene induction in experimental and clinical acute kidney injury. PLoS One 2014; 9: e98380.
Google Scholar | Crossref | Medline39. Bali, KK, Kuner, R. Therapeutic potential for leukocyte elastase in chronic pain states harboring a neuropathic component. Pain 2017; 158: 2243–2258.
Google Scholar | Crossref | Medline