Molecular Mechanisms of Diabetic Kidney Disease

The inflammatory component of diabetic kidney disease has become of great interest in recent years, with genetic and epigenetic variants playing a fundamental role in the initiation and progression of the disease. Cells of the innate immune system play a major role in the pathogenesis of diabetic ki...

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Autores:
Rico-Fontalvo, Jorge
Aroca, Gustavo
Cabrales, José
Daza-Arnedo, Rodrigo
Yánez-Rodríguez, Tomas
Martínez-Ávila, María Cristina
Uparella-Gulfo, Isabella
Raad-Sarabia, María
Tipo de recurso:
Fecha de publicación:
2022
Institución:
Universidad Simón Bolívar
Repositorio:
Repositorio Digital USB
Idioma:
eng
OAI Identifier:
oai:bonga.unisimon.edu.co:20.500.12442/10501
Acceso en línea:
https://hdl.handle.net/20.500.12442/10501
https://doi.org/10.3390/ijms23158668
https://www.mdpi.com/1422-0067/23/15/8668
Palabra clave:
Genetics
Epigenetic
Inflammatory
Innate
Adaptive
Cytokines
Innovation
Rights
openAccess
License
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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oai_identifier_str oai:bonga.unisimon.edu.co:20.500.12442/10501
network_acronym_str USIMONBOL2
network_name_str Repositorio Digital USB
repository_id_str
dc.title.eng.fl_str_mv Molecular Mechanisms of Diabetic Kidney Disease
title Molecular Mechanisms of Diabetic Kidney Disease
spellingShingle Molecular Mechanisms of Diabetic Kidney Disease
Genetics
Epigenetic
Inflammatory
Innate
Adaptive
Cytokines
Innovation
title_short Molecular Mechanisms of Diabetic Kidney Disease
title_full Molecular Mechanisms of Diabetic Kidney Disease
title_fullStr Molecular Mechanisms of Diabetic Kidney Disease
title_full_unstemmed Molecular Mechanisms of Diabetic Kidney Disease
title_sort Molecular Mechanisms of Diabetic Kidney Disease
dc.creator.fl_str_mv Rico-Fontalvo, Jorge
Aroca, Gustavo
Cabrales, José
Daza-Arnedo, Rodrigo
Yánez-Rodríguez, Tomas
Martínez-Ávila, María Cristina
Uparella-Gulfo, Isabella
Raad-Sarabia, María
dc.contributor.author.none.fl_str_mv Rico-Fontalvo, Jorge
Aroca, Gustavo
Cabrales, José
Daza-Arnedo, Rodrigo
Yánez-Rodríguez, Tomas
Martínez-Ávila, María Cristina
Uparella-Gulfo, Isabella
Raad-Sarabia, María
dc.subject.eng.fl_str_mv Genetics
Epigenetic
Inflammatory
Innate
Adaptive
Cytokines
Innovation
topic Genetics
Epigenetic
Inflammatory
Innate
Adaptive
Cytokines
Innovation
description The inflammatory component of diabetic kidney disease has become of great interest in recent years, with genetic and epigenetic variants playing a fundamental role in the initiation and progression of the disease. Cells of the innate immune system play a major role in the pathogenesis of diabetic kidney disease, with a lesser contribution from the adaptive immune cells. Other components such as the complement system also play a role, as well as specific cytokines and chemokines. The inflammatory component of diabetic kidney disease is of great interest and is an active research field, with the hope to find potential innovative therapeutic targets.
publishDate 2022
dc.date.accessioned.none.fl_str_mv 2022-08-04T20:46:33Z
dc.date.available.none.fl_str_mv 2022-08-04T20:46:33Z
dc.date.issued.none.fl_str_mv 2022
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dc.type.spa.spa.fl_str_mv Artículo científico
dc.identifier.issn.none.fl_str_mv 14220067
dc.identifier.uri.none.fl_str_mv https://hdl.handle.net/20.500.12442/10501
dc.identifier.doi.none.fl_str_mv https://doi.org/10.3390/ijms23158668
dc.identifier.url.none.fl_str_mv https://www.mdpi.com/1422-0067/23/15/8668
identifier_str_mv 14220067
url https://hdl.handle.net/20.500.12442/10501
https://doi.org/10.3390/ijms23158668
https://www.mdpi.com/1422-0067/23/15/8668
dc.language.iso.eng.fl_str_mv eng
language eng
dc.rights.*.fl_str_mv Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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dc.rights.accessrights.spa.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv Attribution-NonCommercial-NoDerivatives 4.0 Internacional
http://creativecommons.org/licenses/by-nc-nd/4.0/
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eu_rights_str_mv openAccess
dc.format.mimetype.spa.fl_str_mv pdf
dc.publisher.eng.fl_str_mv MDPI
dc.source.eng.fl_str_mv International Journal of Molecular Sciences
Int. J. Mol. Sci.
dc.source.none.fl_str_mv Vol. 23 No. 15 (2022)
institution Universidad Simón Bolívar
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spelling Rico-Fontalvo, Jorgedb7fe1a8-5530-4479-a566-077a0266f60dAroca, Gustavoe6bdfa35-1a1c-42aa-aee3-89159433d484Cabrales, José6e1ed240-4636-4399-acd4-de06db60021dDaza-Arnedo, Rodrigo928bf6de-8e8b-40e4-9c34-3b53bd369dbfYánez-Rodríguez, Tomasb3919fcd-56b7-4027-bd0b-3af774456329Martínez-Ávila, María Cristina4d473b3b-c2f0-446c-8133-2e59e2077e8dUparella-Gulfo, Isabella3e1b6152-69d6-4110-96b8-5898318e6888Raad-Sarabia, Maríadecb3890-e8db-44d4-adca-c4e9e0836d8b2022-08-04T20:46:33Z2022-08-04T20:46:33Z202214220067https://hdl.handle.net/20.500.12442/10501https://doi.org/10.3390/ijms23158668https://www.mdpi.com/1422-0067/23/15/8668The inflammatory component of diabetic kidney disease has become of great interest in recent years, with genetic and epigenetic variants playing a fundamental role in the initiation and progression of the disease. Cells of the innate immune system play a major role in the pathogenesis of diabetic kidney disease, with a lesser contribution from the adaptive immune cells. Other components such as the complement system also play a role, as well as specific cytokines and chemokines. The inflammatory component of diabetic kidney disease is of great interest and is an active research field, with the hope to find potential innovative therapeutic targets.pdfengMDPIAttribution-NonCommercial-NoDerivatives 4.0 Internacionalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccesshttp://purl.org/coar/access_right/c_abf2International Journal of Molecular SciencesInt. J. Mol. Sci.Vol. 23 No. 15 (2022)GeneticsEpigeneticInflammatoryInnateAdaptiveCytokinesInnovationMolecular Mechanisms of Diabetic Kidney Diseaseinfo:eu-repo/semantics/articleArtículo científicohttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_2df8fbb1Turkmen, K. Inflammation, oxidative stress, apoptosis, and autophagy in diabetes mellitus and diabetic kidney disease: The Four Horsemen of the Apocalypse. Int. Urol. Nephrol. 2017, 49, 837–844.[CrossRef]Samsu, N. Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment. BioMed. Res. Int. 2021, 2021, 1497449.[CrossRef] [PubMed]Tang, S.C.W.; Yiu,W.H. Innate immunity in diabetic kidney disease. Nat. Rev. Nephrol. 2020, 16, 206–222.[CrossRef] [PubMed]Jung, S.W.; Moon, J.Y. The role of inflammation in diabetic kidney disease. Korean J. Intern. Med. 2021, 36, 753–766.[CrossRef]Woroniecka, K.I.; Park, A.S.D.; Mohtat, D.; Thomas, D.B.; Pullman, J.M.; Susztak, K. Transcriptome analysis of human diabetic kidney disease. Diabetes 2011, 60, 2354–2369.[CrossRef] [PubMed]Kiritoshi, S.; Nishikawa, T.; Sonoda, K.; Kukidome, D.; Senokuchi, T.; Matsuo, T.; Matsumura, T.; Tokunaga, H.; Brownlee, M.; Araki, E. Reactive oxygen species from mitochondria induce cyclooxygenase-2 gene expression in human mesangial cells: Potential role in diabetic nephropathy. Diabetes 2003, 52, 2570–2577.[CrossRef] [PubMed]Reidy, K.; Kang, H.M.; Hostetter, T.; Susztak, K. Molecular mechanisms of diabetic kidney disease. J. Clin. Investig. 2014, 124, 2333–2340.[CrossRef]Dubin, R.F.; Rhee, E.P. Proteomics and Metabolomics in Kidney Disease, including Insights into Etiology, Treatment, and Prevention. Clin. J. Am. Soc. Nephrol. 2020, 15, 404–411.[CrossRef] [PubMed]Gu, H.F. Genetic and Epigenetic Studies in Diabetic Kidney Disease. Front. Genet. 2019, 10, 507.[CrossRef]Rico Fontalvo, J. Enfermedad renal diabética: De cara a la prevención, diagnóstico e intervención temprana. Rev. Colomb. Nefrol. 2020, 7, 15–16.[CrossRef]Shao, B.-Y.; Zhang, S.-F.; Li, H.-D.; Meng, X.-M.; Chen, H.-Y. Epigenetics and Inflammation in Diabetic Nephropathy. Front. 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Serum concentrations of symmetric dimethylarginine and creatinine in cats with kidney stones. PLoS ONE 2017, 12, e0174854.[CrossRef] [PubMed]Hall, J.; Yerramilli, M.; Obare, E.; Yu, S.; Jewell, D. Comparison of serum concentrations of symmetric dimethylarginine and creatinine as kidney function biomarkers in healthy geriatric cats fed reduced protein foods enriched with fish oil, L-carnitine, and medium-chain triglycerides. Veter-J. 2014, 202, 588–596. [CrossRef]Hall, J.; Yerramilli, M.; Obare, E.; Yu, S.; Jewell, D. Comparison of serum concentrations of symmetric dimethylarginine and creatinine as kidney function biomarkers in healthy geriatric cats fed reduced protein foods enriched with fish oil, L-carnitine, and medium-chain triglycerides. Veter-J. 2014, 202, 588–596. [CrossRef]Togashi, Y.; Miyamoto, Y. Urinary cystatin C as a biomarker for diabetic nephropathy and its immunohistochemical localization in kidney in Zucker diabetic fatty (ZDF) rats. Exp. Toxicol. Pathol. 2013, 65, 615–622. [CrossRef]van Hoek, I.; Daminet, S.; Notebaert, S.; Janssens, I.; Meyer, E. Immunoassay of urinary retinol binding protein as a putative renal marker in cats. J. Immunol. Methods 2008, 329, 208–213. [CrossRef]Steinbach, S.;Weis, J.; Schweighauser, A.; Francey, T.; Neiger, R. Plasma and Urine Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Dogs with Acute Kidney Injury or Chronic Kidney Disease. J. Veter-Intern. Med. 2014, 28, 264–269. [CrossRef]Hosohata, K.; Ando, H.; Takeshita, Y.; Misu, H.; Takamura, T.; Kaneko, S.; Fujimura, A. Urinary Kim-1 is a sensitive biomarker for the early stage of diabetic nephropathy in Otsuka Long-Evans Tokushima Fatty rats. Diabetes Vasc. Dis. Res. 2014, 11, 243–250. [CrossRef] [PubMed]Colhoun, H.M.; Marcovecchio, M.L. Biomarkers of diabetic kidney disease. Diabetologia 2018, 61, 996–1011. [CrossRef] [PubMed]Carlsson, A.; Östgren, C.; Länne, T.; Larsson, A.; Nystrom, F.; Ärnlöv, J. The association between endostatin and kidney disease and mortality in patients with type 2 diabetes. Diabetes Metab. 2016, 42, 351–357. [CrossRef] [PubMed]Dieter, B.P.; McPherson, S.M.; Afkarian, M.; de Boer, I.H.; Mehrotra, R.; Short, R.; Barbosa-Leiker, C.; Alicic, R.Z.; Meek, R.L.; Tuttle, K.R. Serum amyloid a and risk of death and end-stage renal disease in diabetic kidney disease. J. Diabetes Complicat. 2016, 30, 1467–1472. [CrossRef]Garg, V.; Kumar, M.; Mahapatra, H.S.; Chitkara, A.; Gadpayle, A.K.; Sekhar, V. Novel urinary biomarkers in pre-diabetic nephropathy. Clin. Exp. Nephrol. 2015, 19, 895–900. [CrossRef] [PubMed]Fufaa, G.D.; Weil, E.J.; Nelson, R.G.; Hanson, R.L.; Bonventre, J.V.; Sabbisetti, V.; Waikar, S.S.; Mifflin, T.E.; Zhang, X.; Xie, D.; et al. Association of urinary KIM-1, L-FABP, NAG and NGAL with incident end-stage renal disease and mortality in American Indians with type 2 diabetes mellitus. Diabetologia 2014, 58, 188–198. [CrossRef]Lopes-Virella, M.F.; Baker, N.L.; Hunt, K.J.; Cleary, P.A.; Klein, R.; Virella, G. The DCCT/EDIC Research Group Baseline Markers of Inflammation Are Associated with Progression to Macroalbuminuria in Type 1 Diabetic Subjects. Diabetes Care 2013, 36, 2317–2323. [CrossRef]Araki, S.-I.; Haneda, M.; Koya, D.; Sugaya, T.; Isshiki, K.; Kume, S.; Kashiwagi, A.; Uzu, T.; Maegawa, H. Predictive Effects of Urinary Liver-Type Fatty Acid–Binding Protein for Deteriorating Renal Function and Incidence of Cardiovascular Disease in Type 2 Diabetic Patients without Advanced Nephropathy. Diabetes Care 2013, 36, 1248–1253. [CrossRef]Niewczas, M.A.; Gohda, T.; Skupien, J.; Smiles, A.M.; Walker, W.H.; Rosetti, F.; Cullere, X.; Eckfeldt, J.H.; Doria, A.; Mayadas, T.N.; et al. Circulating TNF Receptors 1 and 2 Predict ESRD in Type 2 Diabetes. J. Am. Soc. Nephrol. 2012, 23, 507–515. 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Systemic immune mediators and lifestyle changes in the prevention of type 2 diabetes: Results from the Finnish Diabetes Prevention Study. Diabetes 2006, 55, 2340–2346. [CrossRef] [PubMed]Flyvbjerg, A. The role of the complement system in diabetic nephropathy. Nat. Rev. Nephrol. 2017, 13, 311–318. [CrossRef] [PubMed]Hajishengallis, G.; Reis, E.S.; Mastellos, D.C.; Ricklin, D.; Lambris, J.D. Novel mechanisms and functions of complement. Nat. Immunol. 2017, 18, 1288–1298. [CrossRef]Tang, S.; Zhou,W.; Sheerin, N.S.; Vaughan, R.W.; Sacks, S.H. Contribution of renal secreted complement C3 to the circulating pool in humans. J Immunol 1999, 162, 4336–4341.Budge, K.; Dellepiane, S.; Yu, S.M.W.; Cravedi, P. Complement, a Therapeutic Target in Diabetic Kidney Disease. Front. Med. 2020, 7, 599236. [CrossRef] [PubMed]Rasmussen, K.L.; Nordestgaard, B.G.; Nielsen, S.F. Complement C3 and Risk of Diabetic Microvascular Disease: A Cohort Study of 95202 Individuals from the General Population. Clin. 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The imbalance of Th17/Th1/Tregs in patients with type 2 diabetes: Relationship with metabolic factors and complications. J. Mol. Med. 2012, 90, 175–186. [CrossRef] [PubMed]Moon, J.Y.; Jeong, K.H.; Lee, T.W.; Ihm, C.G.; Lim, S.J.; Lee, S.H. Aberrant recruitment and activation of T cells in diabetic nephropathy. Am. J. Nephrol. 2012, 35, 164–174. [CrossRef] [PubMed]Selye, H. Production of Nephrosclerosis by Overdosage with Desoxycorticosterone Acetate. Can. Med. Assoc. J. 1942, 47, 515–519. [PubMed]Kang, Y.S.; Cha, D.R. Aldosterone and diabetic kidney disease. Curr. Diab. Rep. 2009, 9, 453–459. [CrossRef] [PubMed]Tuttle, K.R.; Brosius, F.C.; Adler, S.G.; Kretzler, M.; Mehta, R.L.; Tumlin, J.A.; Tanaka, Y.; Haneda, M.; Liu, J.; Silk, M.E.; et al. JAK1/JAK2 inhibition by baricitinib in diabetic kidney disease: Results from a Phase 2 randomized controlled clinical trial. Nephrol. Dial. Transplant. 2018, 33, 1950–1959. 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