Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes

Abstract In this review, we focus specifically on the role that the metalloproteinase, A Disintegrin and Metalloproteinase 17 [ADAM17] plays in the development and progression of the metabolic syndrome. There is a well-recognised link between the ADAM17 substrate tumour necrosis factor α (TNF-α) and obesity, inflammation and diabetes. In addition, knocking out ADAM17 in mice leads to an extremely lean phenotype. Importantly, ADAM17-deficient mice exhibit one of the most pronounced examples of hypermetabolism in rodents to date. It is vital to further understand the mechanistic role that ADAM17 plays in the metabolic syndrome. Such studies will demonstrate that ADAM17 is a valuable therapeutic target to treat obesity and diabetes.

[1]  A. Magno,et al.  SGLT2 Inhibitor-Induced Sympathoexcitation in White Adipose Tissue: A Novel Mechanism for Beiging , 2020, Biomedicines.

[2]  E. Lazartigues,et al.  ADAM17-Mediated Shedding of Inflammatory Cytokines in Hypertension , 2020, Frontiers in Pharmacology.

[3]  G. Duan,et al.  Prognostic Significance of ADAM17 for Gastric Cancer Survival: A Meta-Analysis , 2020, Medicina.

[4]  R. Wong,et al.  Trends in the Prevalence of Metabolic Syndrome in the United States, 2011-2016. , 2020, JAMA.

[5]  Quynh Nguyen,et al.  Angiotensin-Converting Enzyme 2: SARS-CoV-2 Receptor and Regulator of the Renin-Angiotensin System , 2020, Circulation research.

[6]  D. Meyerholz,et al.  Loss of iRhom2 accelerates fat gain and insulin resistance in diet-induced obesity despite reduced adipose tissue inflammation. , 2020, Metabolism: clinical and experimental.

[7]  D. Gutsaeva,et al.  Role of Endothelial ADAM17 in Early Vascular Changes Associated with Diabetic Retinopathy , 2020, Journal of clinical medicine.

[8]  R. de Mutsert,et al.  The prevalence of metabolic syndrome and its association with body fat distribution in middle-aged individuals from Indonesia and the Netherlands: a cross-sectional analysis of two population-based studies , 2020, Diabetology & Metabolic Syndrome.

[9]  T. Sasase,et al.  A Novel TNF-α Converting Enzyme (TACE) Selective Inhibitor JTP-96193 Prevents Insulin Resistance in KK-Ay Type 2 Diabetic Mice and Diabetic Peripheral Neuropathy in Type 1 Diabetic Mice. , 2019, Biological & pharmaceutical bulletin.

[10]  Qingchun Zhao,et al.  Novel ADAM-17 inhibitor ZLDI-8 inhibits the proliferation and metastasis of chemo-resistant non-small-cell lung cancer by reversing Notch and epithelial mesenchymal transition in vitro and in vivo. , 2019, Pharmacological research.

[11]  J. Pascual,et al.  Role of ADAM17 in kidney disease. , 2019, American journal of physiology. Renal physiology.

[12]  A. Ludwig,et al.  Status update on iRhom and ADAM17: It's still complicated. , 2019, Biochimica et biophysica acta. Molecular cell research.

[13]  A. Zsombok,et al.  Activation of ADAM17 (A Disintegrin and Metalloprotease 17) on Glutamatergic Neurons Selectively Promotes Sympathoexcitation , 2019, Hypertension.

[14]  N. Ward,et al.  SGLT2 Inhibitor–Induced Sympathoinhibition , 2019, JACC. Basic to translational science.

[15]  Linfeng Hu,et al.  iRhom2 serves as a facilitator in obesity by enhancing adipose inflammation and insulin resistance , 2019 .

[16]  J. Padilla,et al.  ADAM17 Cleaves the Insulin Receptor α‐Subunit on Endothelial Cells and Induces Vascular Insulin Resistance in Type 2 Diabetes , 2019, The FASEB Journal.

[17]  Haibo Zhou,et al.  Inhibition of hepatocellular carcinoma cell proliferation, migration, and invasion by a disintegrin and metalloproteinase-17 inhibitor TNF484 , 2019, Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences.

[18]  M. Freeman,et al.  The molecular, cellular and pathophysiological roles of iRhom pseudoproteases , 2019, Open Biology.

[19]  J. Bereta,et al.  The role of NF-κB and Elk-1 in the regulation of mouse ADAM17 expression , 2019, Biology Open.

[20]  M. D. Turner,et al.  Type 2 diabetes - An autoinflammatory disease driven by metabolic stress. , 2018, Biochimica et biophysica acta. Molecular basis of disease.

[21]  H. Hammad,et al.  The emerging role of ADAM metalloproteinases in immunity , 2018, Nature Reviews Immunology.

[22]  T. Kasama,et al.  ADAM-17 is expressed on rheumatoid arthritis fibroblast-like synoviocytes and regulates proinflammatory mediator expression and monocyte adhesion , 2018, Arthritis Research & Therapy.

[23]  Michelle K. Lupton,et al.  A rare loss-of-function variant of ADAM17 is associated with late-onset familial Alzheimer disease , 2018, Molecular Psychiatry.

[24]  Jessica M. Overstreet,et al.  Inhibition of Epidermal Growth Factor Receptor Activation Is Associated With Improved Diabetic Nephropathy and Insulin Resistance in Type 2 Diabetes , 2018, Diabetes.

[25]  D. Schmidt-Arras,et al.  ADAM17 inhibition enhances platinum efficiency in ovarian cancer , 2018, Oncotarget.

[26]  B. Scholte,et al.  The EGFR-ADAM17 Axis in Chronic Obstructive Pulmonary Disease and Cystic Fibrosis Lung Pathology , 2018, Mediators of inflammation.

[27]  M. Moss,et al.  Recent Advances in ADAM17 Research: A Promising Target for Cancer and Inflammation , 2017, Mediators of inflammation.

[28]  Y. Okada,et al.  The Metalloproteinase ADAM28 Promotes Metabolic Dysfunction in Mice , 2017, International journal of molecular sciences.

[29]  J. Blangero,et al.  ADAM19: A Novel Target for Metabolic Syndrome in Humans and Mice , 2017, Mediators of inflammation.

[30]  R. Jayawardena,et al.  Prevalence and trends of metabolic syndrome among adults in the asia-pacific region: a systematic review , 2017, BMC Public Health.

[31]  S. Waikar,et al.  ADAM17 substrate release in proximal tubule drives kidney fibrosis. , 2016, JCI insight.

[32]  Stefan Rose-John,et al.  IL-6 pathway in the liver: From physiopathology to therapy. , 2016, Journal of hepatology.

[33]  K. Reiss,et al.  Phosphatidylserine exposure is required for ADAM17 sheddase function , 2016, Nature Communications.

[34]  O. Riesterer,et al.  Secretome Signature Identifies ADAM17 as Novel Target for Radiosensitization of Non–Small Cell Lung Cancer , 2016, Clinical Cancer Research.

[35]  B. Zinman,et al.  Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. , 2015, The New England journal of medicine.

[36]  C. Tack,et al.  IL-1 family members in the pathogenesis and treatment of metabolic disease: Focus on adipose tissue inflammation and insulin resistance. , 2015, Cytokine.

[37]  M. Reilly,et al.  Metabolic Effects of CX3CR1 Deficiency in Diet-Induced Obese Mice , 2015, PloS one.

[38]  Peter F. Wright,et al.  Shedding of TNF receptor 2 by effector CD8+ T cells by ADAM17 is important for regulating TNF‐α availability during influenza infection , 2015, Journal of leukocyte biology.

[39]  H. Bahudhanapati,et al.  Evolution of Vertebrate Adam Genes; Duplication of Testicular Adams from Ancient Adam9/9-like Loci , 2015, PloS one.

[40]  M. Charbonneau,et al.  High Glucose Up-regulates ADAM17 through HIF-1α in Mesangial Cells* , 2015, The Journal of Biological Chemistry.

[41]  W. Shi,et al.  Blocking IL-6 trans-signaling prevents high-fat diet-induced adipose tissue macrophage recruitment but does not improve insulin resistance. , 2015, Cell metabolism.

[42]  S. Uhlig,et al.  ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets. , 2015, American journal of physiology. Lung cellular and molecular physiology.

[43]  K. Horiuchi,et al.  ADAM17 regulates IL-1 signaling by selectively releasing IL-1 receptor type 2 from the cell surface. , 2015, Cytokine.

[44]  Xueyao Yin,et al.  Circulating Fractalkine Levels Predict the Development of the Metabolic Syndrome , 2014, International journal of endocrinology.

[45]  Kavaljit H. Chhabra,et al.  Brain Angiotensin-Converting Enzyme Type 2 Shedding Contributes to the Development of Neurogenic Hypertension , 2013, Circulation research.

[46]  M. Federici,et al.  The role of ADAM17 in metabolic inflammation. , 2013, Atherosclerosis.

[47]  C. Cho.  Testicular and epididymal ADAMs: expression and function during fertilization , 2012, Nature Reviews Urology.

[48]  J. Blangero,et al.  ADAM28 is elevated in humans with the metabolic syndrome and is a novel sheddase of human tumour necrosis factor‐α , 2012, Immunology and cell biology.

[49]  K. Horiuchi,et al.  Tumor necrosis factor-α converting enzyme inactivation ameliorates high-fat diet-induced insulin resistance and altered energy homeostasis. , 2011, Circulation journal : official journal of the Japanese Circulation Society.

[50]  Mingyao Li,et al.  Fractalkine Is a Novel Human Adipochemokine Associated With Type 2 Diabetes , 2011, Diabetes.

[51]  R. Hynes,et al.  The Lack of ADAM17 Activity during Embryonic Development Causes Hemorrhage and Impairs Vessel Formation , 2010, PloS one.

[52]  K. Horiuchi,et al.  Ectodomain shedding of EGFR ligands and TNFR1 dictates hepatocyte apoptosis during fulminant hepatitis in mice. , 2010, The Journal of clinical investigation.

[53]  M. Gooz.  ADAM-17: the enzyme that does it all , 2010, Critical reviews in biochemistry and molecular biology.

[54]  J. Scheller,et al.  ADAM17-mediated shedding of the IL6R induces cleavage of the membrane stub by gamma-secretase. , 2010, Biochimica et biophysica acta.

[55]  S. Menini,et al.  Increased tumor necrosis factor α–converting enzyme activity induces insulin resistance and hepatosteatosis in mice , 2010, Hepatology.

[56]  M. Chopp,et al.  Transcription factor Sp1 induces ADAM17 and contributes to tumor cell invasiveness under hypoxia , 2009, Journal of experimental & clinical cancer research : CR.

[57]  Paul L. Huang.  A comprehensive definition for metabolic syndrome , 2009, Disease Models & Mechanisms.

[58]  B. Walcheck,et al.  Regulation of Mature ADAM17 by Redox Agents for L-Selectin Shedding1 , 2009, The Journal of Immunology.

[59]  L. Cassis,et al.  ACE2 is expressed in mouse adipocytes and regulated by a high-fat diet. , 2008, American journal of physiology. Regulatory, integrative and comparative physiology.

[60]  P. Dempsey,et al.  Deficiency of TNFalpha converting enzyme (TACE/ADAM17) causes a lean, hypermetabolic phenotype in mice. , 2008, Endocrinology.

[61]  M. Alessi,et al.  Microparticles of human atherosclerotic plaques enhance the shedding of the tumor necrosis factor-alpha converting enzyme/ADAM17 substrates, tumor necrosis factor and tumor necrosis factor receptor-1. , 2007, The American journal of pathology.

[62]  M. Federici,et al.  Mice Heterozygous for Tumor Necrosis Factor-α Converting Enzyme Are Protected From Obesity-Induced Insulin Resistance and Diabetes , 2007, Diabetes.

[63]  J. Trzăskos,et al.  Pharmacokinetics and Pharmacodynamics of DPC 333 ((2R)-2-((3R)-3-Amino-3{4-[2-methyl-4-quinolinyl) methoxy] phenyl}-2-oxopyrrolidinyl)-N-hydroxy-4-methylpentanamide)), a Potent and Selective Inhibitor of Tumor Necrosis Factor α-Converting Enzyme in Rodents, Dogs, Chimpanzees, and Humans , 2007, Drug Metabolism and Disposition.

[64]  H. Sul,et al.  Pref-1, a preadipocyte secreted factor that inhibits adipogenesis. , 2006, The Journal of nutrition.

[65]  É. Hajduch,et al.  IL‐1 receptor antagonist in metabolic diseases: Dr Jekyll or Mr Hyde? , 2006, FEBS letters.

[66]  H. Sul,et al.  Ectodomain Shedding of Preadipocyte Factor 1 (Pref-1) by Tumor Necrosis Factor Alpha Converting Enzyme (TACE) and Inhibition of Adipocyte Differentiation , 2006, Molecular and Cellular Biology.

[67]  G. Weskamp,et al.  Distinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligands , 2004, The Journal of cell biology.

[68]  M. Kaler,et al.  Release of full-length 55-kDa TNF receptor 1 in exosome-like vesicles: a mechanism for generation of soluble cytokine receptors. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[69]  Claude Lenfant,et al.  Definition of Metabolic Syndrome: Report of the National Heart, Lung, and Blood Institute/American Heart Association Conference on Scientific Issues Related to Definition , 2004, Arteriosclerosis, thrombosis, and vascular biology.

[70]  Stefan Rose-John,et al.  Cellular Cholesterol Depletion Triggers Shedding of the Human Interleukin-6 Receptor by ADAM10 and ADAM17 (TACE)* , 2003, Journal of Biological Chemistry.

[71]  C. Blobel,et al.  Tumor necrosis factor-alpha-converting enzyme (ADAM17) mediates the cleavage and shedding of fractalkine (CX3CL1). , 2001, The Journal of biological chemistry.

[72]  B. Baker,et al.  ADAM17 but not ADAM10 mediates tumor necrosis factor-alpha and L-selectin shedding from leukocyte membranes. , 2001, Antisense & nucleic acid drug development.

[73]  David C. Lee,et al.  An essential role for ectodomain shedding in mammalian development. , 1998, Science.

[74]  Nicole Nelson,et al.  A metalloproteinase disintegrin that releases tumour-necrosis factor-α from cells , 1997, Nature.

[75]  R. Black,et al.  A metalloprotease inhibitor blocks shedding of the 80-kD TNF receptor and TNF processing in T lymphocytes , 1995, The Journal of experimental medicine.

[76]  D. Goeddel,et al.  Biochemical properties of the 75-kDa tumor necrosis factor receptor. Characterization of ligand binding, internalization, and receptor phosphorylation. , 1992, The Journal of biological chemistry.

[77]  内川 伸一.  ADAM17 regulates IL-1 signaling by selectively releasing IL-1 receptor type 2 from the cell surface , 2015 .

[78]  G. Oudit,et al.  Angiotensin II induced proteolytic cleavage of myocardial ACE2 is mediated by TACE/ADAM-17: a positive feedback mechanism in the RAS. , 2014, Journal of molecular and cellular cardiology.

[79]  D. Seals,et al.  The ADAMs family of metalloproteases: multidomain proteins with multiple functions. , 2003, Genes & development.

[80]  E. Ayaşlıoğlu,et al.  Cytokine inhibitors: soluble tumor necrosis factor receptor 1 and interleukin-1 receptor antagonist in Behçet’s disease , 2003, Rheumatology International.