Generic placeholder image

Current Diabetes Reviews

Editor-in-Chief

ISSN (Print): 1573-3998
ISSN (Online): 1875-6417

Review Article

The Functional Role of microRNAs and mRNAs in Diabetic Kidney Disease: A Review

Author(s): Bhuvnesh Rai*, Jyotika Srivastava and Pragati Saxena

Volume 20, Issue 6, 2024

Published on: 20 October, 2023

Article ID: e201023222412 Pages: 9

DOI: 10.2174/0115733998270983231009094216

Price: $65

Abstract

Diabetes is a group of diseases marked by poor control of blood glucose levels. Diabetes mellitus (DM) occurs when pancreatic cells fail to make insulin, which is required to keep blood glucose levels stable, disorders, and so on. High glucose levels in the blood induce diabetic effects, which can cause catastrophic damage to bodily organs such as the eyes and lower extremities. Diabetes is classified into many forms, one of which is controlled by hyperglycemia or Diabetic Kidney Disease (DKD), and another that is not controlled by hyperglycemia (nondiabetic kidney disease or NDKD) and is caused by other factors such as hypertension, hereditary. DKD is associated with diabetic nephropathy (DN), a leading cause of chronic kidney disease (CKD) and end-stage renal failure. The disease is characterized by glomerular basement membrane thickening, glomerular sclerosis, and mesangial expansion, resulting in a progressive decrease in glomerular filtration rate, glomerular hypertension, and renal failure or nephrotic syndrome. It is also represented by some microvascular complications such as nerve ischemia produced by intracellular metabolic changes, microvascular illness, and the direct impact of excessive blood glucose on neuronal activity. Therefore, DKD-induced nephrotic failure is worse than NDKD.

MicroRNAs (miRNAs) are important in the development and progression of several diseases, including diabetic kidney disease (DKD). These dysregulated miRNAs can impact various cellular processes, including inflammation, fibrosis, oxidative stress, and apoptosis, all of which are implicated during DKD. MiRNAs can alter the course of DKD by targeting several essential mechanisms. Understanding the miRNAs implicated in DKD and their involvement in disease development might lead to identifying possible therapeutic targets for DKD prevention and therapy. Therefore, this review focuses specifically on DKD-associated DN, as well as how in-silico approaches may aid in improving the management of the disease.

[1]
Lin X, Xu Y, Pan X, et al. Global, regional, and national burden and trend of diabetes in 195 countries and territories: An analysis from 1990 to 2025. Sci Rep 2020; 10(1): 14790.
[http://dx.doi.org/10.1038/s41598-020-71908-9] [PMID: 32901098]
[2]
Saeedi P. Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9th edition. Diabetes Res Clin Pract 2019; 157: 107843.
[3]
Sami W, Ansari T, Butt NS, Hamid MRA. Effect of diet on type 2 diabetes mellitus: A review. Int J Health Sci 2017; 11(2): 65-71.
[PMID: 28539866]
[4]
Holman N, Young B, Gadsby R. Current prevalence of Type 1 and Type 2 diabetes in adults and children in the UK. Diabet Med 2015; 32(9): 1119-20.
[http://dx.doi.org/10.1111/dme.12791] [PMID: 25962518]
[5]
Bruno G, Runzo C, Cavallo-Perin P, et al. Incidence of type 1 and type 2 diabetes in adults aged 30-49 years: the population-based registry in the province of Turin, Italy. Diabetes Care 2005; 28(11): 2613-9.
[http://dx.doi.org/10.2337/diacare.28.11.2613] [PMID: 16249528]
[6]
India’s diabetes epidemic cuts down millions who escape poverty. Bloomberg 2010.
[7]
Burrack AL, Martinov T, Fife BT. T cell-mediated beta cell destruction: Autoimmunity and alloimmunity in the context of type 1 diabetes. Front Endocrinol 2017; 8: 343.
[http://dx.doi.org/10.3389/fendo.2017.00343] [PMID: 29259578]
[8]
Tshivhase A, Matsha T, Raghubeer S. Diagnosis and treatment of MODY: An updated mini review. Appl Sci 2021; 11(20): 9436.
[http://dx.doi.org/10.3390/app11209436]
[9]
Cade WT. Diabetes-related microvascular and macrovascular diseases in the physical therapy setting. Phys Ther 2008; 88(11): 1322-35.
[http://dx.doi.org/10.2522/ptj.20080008] [PMID: 18801863]
[10]
Anjali DD, Harris-Hayes M, Mario S. Epidemiology of diabetes and diabetes-related complications. Phys Ther 2008; 88(11): 1254-64.
[11]
Farida C, Said A, Souad M. Diabetes mellitus in elderly. Indian J Endocrinol Metab 2015; 19(6): 744-52.
[12]
Lim A. Diabetic nephropathy - complications and treatment. Int J Nephrol Renovasc Dis 2014; 7: 361-81.
[http://dx.doi.org/10.2147/IJNRD.S40172] [PMID: 25342915]
[13]
Radica ZA, Michele TR, Katherine RT. Diabetic kidney disease: Challenges, progress, and possibilities. Clin J Am Soc Nephrol 2017; 12(12): 2032-45.
[14]
Chawla R, Chawla A, Jaggi S. Microvasular and macrovascular complications in diabetes mellitus: Distinct or continuum? Indian J Endocrinol Metab 2016; 20(4): 546-51.
[http://dx.doi.org/10.4103/2230-8210.183480] [PMID: 27366724]
[15]
Tracy JA, Dyck PJB. The spectrum of diabetic neuropathies. Phys Med Rehabil Clin N Am 2008; 19: 1-26.
[http://dx.doi.org/10.1016/j.pmr.2007.10.010]
[16]
Yi T, Zhiguo Z, Chao Z, et al. Mechanisms of diabetic cardiomyopathy and potential therapeutic strategies: Preclinical and clinical evidence. Nat Rev Cardiol 2020; 17(9): 585-607.
[17]
Ahmet AK, Halis KA, Timir KP. Diabetes, cardiomyopathy, and heart failure.
[18]
Rodrigues C, Rodrigues M, Henriques M. Candida sp. infections in patients with diabetes mellitus. J Clin Med 2019; 8(1): 76.
[http://dx.doi.org/10.3390/jcm8010076] [PMID: 30634716]
[19]
Rosen J, Yosipovitch G. Skin manifestations of diabetes mellitus. Endotext. MDText.com, Inc 2000.
[20]
Casqueiro J, Casqueiro J, Alves C. Infections in patients with diabetes mellitus: A review of pathogenesis. Indian J Endocrinol Metab 2012; 16(S1): S27-36.
[PMID: 22701840]
[21]
Shaheen T, Naim A, Osama H. Nonalcoholic fatty liver disease and type 2 diabetes: Where do diabetologists stand? Clin Diabetes Endocrinol 2020; 6: 9.
[22]
Wenjie D, Ling Y, Aizhong L. Prevalence of nonalcoholic fatty liver disease in patients with type 2 diabetes mellitus: A meta-analysis. Medicine 2017; 96(39): e8179.
[23]
Mohamed L, Jennifer A, Kalasz H. Chronic complications of diabetes mellitus: A mini review. Curr Diabetes Rev 13(1): 3-10.
[24]
Mauer AM, Steffes MW, Brown DM. The kidney in diabetes. Am J Med 1981; 70(3): 603-6012.
[25]
Allison JH, Mark EM. Management of diabetes mellitus in patients with chronic kidney disease. Clin Diabetes Endocrinol 2015; 1.
[26]
Shahbazian H. Diabetic kidney disease; review of the current knowledge. J Renal Inj Prev 2013; 2(2): 73-80.
[http://dx.doi.org/10.12861/jrip.2013.24]
[27]
DeFronzo RA, Reeves WB, Awad AS. Pathophysiology of diabetic kidney disease: Impact of SGLT2 inhibitors. Nat Rev Nephrol 2021; 17(5): 319-34.
[http://dx.doi.org/10.1038/s41581-021-00393-8] [PMID: 33547417]
[28]
Dabla PK. Renal function in diabetic nephropathy. World J Diabetes 2010; 1(2): 48-56.
[http://dx.doi.org/10.4239/wjd.v1.i2.48] [PMID: 21537427]
[29]
Gheith O, Farouk N, Nampoory N, Halim MA, Al-Otaibi T. Diabetic kidney disease: World wide difference of prevalence and risk factors. J Nephropharmacol 2015; 5(1): 49-56.
[PMID: 28197499]
[30]
Barrera-Chimal J, Jaisser F. Pathophysiologic mechanisms in diabetic kidney disease: A focus on current and future therapeutic targets. Diabetes Obes Metab 2020; 22(S1): 16-31.
[http://dx.doi.org/10.1111/dom.13969] [PMID: 32267077]
[31]
Peti-Peterdi J, Raymond CH. Macula densa sensing and signaling mechanisms of renin release. J Am Soc Nephrol 2010; 21(7): 1093-6.
[32]
Inscho EW, Imig JD, Cook AK. Afferent and efferent arteriolar vasoconstriction to angiotensin II and norepinephrine involves release of Ca2+ from intracellular stores. Hypertension 1997; 29(1): 222-7.
[http://dx.doi.org/10.1161/01.HYP.29.1.222] [PMID: 9039106]
[33]
Sara G, David B, Mark EC. Mechanisms of diabetic nephropathy: Role of hypertension. Hypertension 2006; 48(4): 519-26.
[34]
Zhou Y, Liao Q, Luo Y, Qing Z, Zhang Q, He G. Renal protective effect of Rosa laevigata Michx. by the inhibition of oxidative stress in streptozotocin-induced diabetic rats. Mol Med Rep 2012; 5(6): 1548-54.
[PMID: 22469771]
[35]
Yamagishi S, Nakamura N, Suematsu M, Kaseda K, Matsui T. Advanced glycation end products: A molecular target for vascular complications in diabetes. Mol Med 2015; 21(S1): S32-40.
[http://dx.doi.org/10.2119/molmed.2015.00067] [PMID: 26605646]
[36]
Garud M, Kulkarni Y. Hyperglycemia to nephropathy via transforming growth factor beta. Curr Diabetes Rev 2014; 10(3): 182-9.
[http://dx.doi.org/10.2174/1573399810666140606103645] [PMID: 24919657]
[37]
Awad AS, You H, Gao T, et al. Macrophage-derived tumor necrosis factor-α mediates diabetic renal injury. Kidney Int 2015; 88(4): 722-33.
[http://dx.doi.org/10.1038/ki.2015.162] [PMID: 26061548]
[38]
Chow F, Ozols E, Nikolic-Paterson DJ, Atkins RC, Tesch GH. Macrophages in mouse type 2 diabetic nephropathy: Correlation with diabetic state and progressive renal injury. Kidney Int 2004; 65(1): 116-28.
[http://dx.doi.org/10.1111/j.1523-1755.2004.00367.x] [PMID: 14675042]
[39]
Calle P, Hotter G. Macrophage phenotype and fibrosis in diabetic nephropathy. Int J Mol Sci 2020; 21(8): 2806.
[http://dx.doi.org/10.3390/ijms21082806] [PMID: 32316547]
[40]
Pugliese G, Penno G, Natali A, et al. Diabetic kidney disease: New clinical and therapeutic issues. Joint position statement of the Italian Diabetes Society and the Italian Society of Nephrology on “The natural history of diabetic kidney disease and treatment of hyperglycemia in patients with type 2 diabetes and impaired renal function”. J Nephrol 2020; 33(1): 9-35.
[http://dx.doi.org/10.1007/s40620-019-00650-x] [PMID: 31576500]
[41]
Esteller M. Non-coding RNAs in human disease. Nat Rev Genet 2011; 12(12): 861-74.
[http://dx.doi.org/10.1038/nrg3074] [PMID: 22094949]
[42]
Butz H, Kinga N, Racz K, Patocs A. Circulating miRNAs as biomarkers for endocrine disorders. J Endocrinol Invest 2016; 39(1): 1-10.
[http://dx.doi.org/10.1007/s40618-015-0316-5] [PMID: 26015318]
[43]
Andrey T, William CC. The origin, function and diagnostic potential of extracellular microRNA in human body fluids. Front Genet 2014; 5.
[44]
Esquela-Kerscher A, Slack FJ. Oncomirs — microRNAs with a role in cancer. Nat Rev Cancer 2006; 6(4): 259-69.
[http://dx.doi.org/10.1038/nrc1840] [PMID: 16557279]
[45]
Janssen HLA, Reesink HW, Lawitz EJ, et al. Treatment of HCV infection by targeting microRNA. N Engl J Med 2013; 368(18): 1685-94.
[http://dx.doi.org/10.1056/NEJMoa1209026] [PMID: 23534542]
[46]
Chang TC, Mendell JT. microRNAs in vertebrate physiology and human disease. Annu Rev Genomics Hum Genet 2007; 8(1): 215-39.
[http://dx.doi.org/10.1146/annurev.genom.8.080706.092351] [PMID: 17506656]
[47]
Chen CZ. MicroRNAs as oncogenes and tumor suppressors. N Engl J Med 2005; 353(17): 1768-71.
[http://dx.doi.org/10.1056/NEJMp058190] [PMID: 16251533]
[48]
Hennessy E, O’Driscoll L. Molecular medicine of microRNAs: Structure, function and implications for diabetes. Expert Rev Mol Med 2008; 10: e24.
[http://dx.doi.org/10.1017/S1462399408000781] [PMID: 18702835]
[49]
Saal S, Harvey SJ. MicroRNAs and the kidney: Coming of age. Curr Opin Nephrol Hypertens 2009; 18(4): 317-23.
[http://dx.doi.org/10.1097/MNH.0b013e32832c9da2] [PMID: 19424061]
[50]
Kato M, Natarajan R. microRNA cascade in diabetic kidney disease: Big impact initiated by a small RNA. Cell Cycle 2009; 8(22): 3613-4.
[http://dx.doi.org/10.4161/cc.8.22.9816] [PMID: 19884793]
[51]
Kato M, Arce L, Natarajan R. MicroRNAs and their role in progressive kidney diseases. Clin J Am Soc Nephrol 2009; 4(7): 1255-66.
[http://dx.doi.org/10.2215/CJN.00520109] [PMID: 19581401]
[52]
Kaucsár T, Rácz Z, Hamar P. Post-transcriptional gene-expression regulation by micro RNA (miRNA) network in renal disease. Adv Drug Deliv Rev 2010; 62(14): 1390-401.
[http://dx.doi.org/10.1016/j.addr.2010.10.003] [PMID: 20940025]
[53]
Akkina S, Becker BN. MicroRNAs in kidney function and disease. Transl Res 2011; 157(4): 236-40.
[http://dx.doi.org/10.1016/j.trsl.2011.01.011] [PMID: 21420034]
[54]
Ho J, Kreidberg JA. The long and short of microRNAs in the kidney. J Am Soc Nephrol 2012; 23(3): 400-4.
[http://dx.doi.org/10.1681/ASN.2011080797] [PMID: 22302196]
[55]
Chandrasekaran K, Karolina DS, Sepramaniam S, et al. Role of microRNAs in kidney homeostasis and disease. Kidney Int 2012; 81(7): 617-27.
[http://dx.doi.org/10.1038/ki.2011.448] [PMID: 22237749]
[56]
Ma L, Qu L. The function of microRNAs in renal development and pathophysiology. J Genet Genomics 2013; 40(4): 143-52.
[http://dx.doi.org/10.1016/j.jgg.2013.03.002] [PMID: 23618397]
[57]
Chung AC, Yu X, Lan HY. MicroRNA and nephropathy: Emerging concepts. Int J Nephrol Renovasc Dis 2013; 6: 169-79.
[PMID: 24109192]
[58]
Jia Y, Guan M, Zheng Z, et al. miRNAs in urine extracellular vesicles as predictors of early-stage diabetic nephropathy. J Diabetes Res 2016; 2016: 1-10.
[http://dx.doi.org/10.1155/2016/7932765] [PMID: 26942205]
[59]
Eissa S, Matboli M, Aboushahba R, Bekhet MM, Soliman Y. Urinary exosomal microRNA panel unravels novel biomarkers for diagnosis of type 2 diabetic kidney disease. J Diabetes Complications 2016; 30(8): 1585-92.
[http://dx.doi.org/10.1016/j.jdiacomp.2016.07.012] [PMID: 27475263]
[60]
Cardenas-Gonzalez M, Srivastava A, Pavkovic M, et al. Identification, confirmation, and replication of novel urinary microrna biomarkers in lupus nephritis and diabetic nephropathy. Clin Chem 2017; 63(9): 1515-26.
[http://dx.doi.org/10.1373/clinchem.2017.274175] [PMID: 28667184]
[61]
Baker MA, Davis SJ, Liu P, et al. Tissue-Specific MicroRNA expression patterns in four types of kidney disease. J Am Soc Nephrol 2017; 28(10): 2985-92.
[http://dx.doi.org/10.1681/ASN.2016121280] [PMID: 28663230]
[62]
Barutta F, Tricarico M, Corbelli A, et al. Urinary exosomal microRNAs in incipient diabetic nephropathy. PLoS One 2013; 8(11): e73798.
[http://dx.doi.org/10.1371/journal.pone.0073798] [PMID: 24223694]
[63]
Argyropoulos C, Wang K, Bernardo J, et al. Urinary microrna profiling predicts the development of microalbuminuria in patients with type 1 diabetes. J Clin Med 2015; 4(7): 1498-517.
[http://dx.doi.org/10.3390/jcm4071498] [PMID: 26239688]
[64]
Argyropoulos C, Wang K, McClarty S, et al. Urinary microRNA profiling in the nephropathy of type 1 diabetes. PLoS One 2013; 8(1): e54662.
[http://dx.doi.org/10.1371/journal.pone.0054662] [PMID: 23358711]
[65]
Kato M, Natarajan R. MicroRNAs in diabetic nephropathy: Functions, biomarkers, and therapeutic targets. Ann N Y Acad Sci 2015; 1353(1): 72-88.
[http://dx.doi.org/10.1111/nyas.12758] [PMID: 25877817]
[66]
Shi S, Yu L, Chiu C, et al. Podocyte-selective deletion of dicer induces proteinuria and glomerulosclerosis. J Am Soc Nephrol 2008; 19(11): 2159-69.
[http://dx.doi.org/10.1681/ASN.2008030312] [PMID: 18776119]
[67]
Ho J, Ng KH, Rosen S, Dostal A, Gregory RI, Kreidberg JA. Podocyte-specific loss of functional microRNAs leads to rapid glomerular and tubular injury. J Am Soc Nephrol 2008; 19(11): 2069-75.
[http://dx.doi.org/10.1681/ASN.2008020162] [PMID: 18832437]
[68]
Harvey SJ, Jarad G, Cunningham J, et al. Podocyte-specific deletion of dicer alters cytoskeletal dynamics and causes glomerular disease. J Am Soc Nephrol 2008; 19(11): 2150-8.
[http://dx.doi.org/10.1681/ASN.2008020233] [PMID: 18776121]
[69]
Kato M, Putta S, Wang M, et al. TGF-β activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN. Nat Cell Biol 2009; 11(7): 881-9.
[http://dx.doi.org/10.1038/ncb1897] [PMID: 19543271]
[70]
Kato M, Arce L, Wang M, Putta S, Lanting L, Natarajan R. A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells. Kidney Int 2011; 80(4): 358-68.
[http://dx.doi.org/10.1038/ki.2011.43] [PMID: 21389977]
[71]
Jung TP, Mitsuo K, Hang Y, et al. FOG2 protein down-regulation by transforming growth factor-β1-induced microrna-200b/c leads to akt kinase activation and glomerular mesangial hypertrophy related to diabetic nephropathy. J Biol Chem 2013; 288(31): 22469-80.
[72]
Mitsuo K, Jane Z, Mei W. MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors. Proc Natl Acad Sci USA 2007; 104(9): 3432-7.
[73]
Zhengwei M, Lin L, Man JL. p53/microRNA-214/ULK1 axis impairs renal tubular autophagy in diabetic kidney disease. J Clin Invest 2020; 130(9): 5011-26.
[74]
Yan-Lin Y, Yang MX, Yi-Jie J. Long noncoding RNA NEAT1 is involved in the protective effect of Klotho on renal tubular epithelial cells in diabetic kidney disease through the ERK1/2 signaling pathway. Exp Mol Med 2020; 52: 266-80.
[75]
Yang YL, Hu F, Xue M, et al. Early growth response protein-1 upregulates long noncoding RNA Arid2-IR to promote extracellular matrix production in diabetic kidney disease. Am J Physiol Cell Physiol 2019; 316(3): C340-52.
[http://dx.doi.org/10.1152/ajpcell.00167.2018] [PMID: 30462533]
[76]
Hu M, Wang R, Li X, et al. LncRNA MALAT1 is dysregulated in diabetic nephropathy and involved in high glucose-induced podocyte injury via its interplay with β-catenin. J Cell Mol Med 2017; 21(11): 2732-47.
[http://dx.doi.org/10.1111/jcmm.13189] [PMID: 28444861]
[77]
Li A, Peng R, Sun Y, Liu H, Peng H, Zhang Z. LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling. Cell Death Dis 2018; 9(5): 461.
[http://dx.doi.org/10.1038/s41419-018-0527-8]
[78]
Weiping Xia, Yao H, Yu G. Long non-coding RNA: An emerging contributor and potential therapeutic target in renal fibrosis. Front Genet 2021; 12.
[79]
Long J, Wang Y, Wang W, Chang BHJ, Danesh FR. MicroRNA-29c is a signature microRNA under high glucose conditions that targets Sprouty homolog 1, and its in vivo knockdown prevents progression of diabetic nephropathy. J Biol Chem 2011; 286(13): 11837-48.
[http://dx.doi.org/10.1074/jbc.M110.194969] [PMID: 21310958]
[80]
Mu J, Pang Q, Guo YH. Functional implications of MicroRNA-215 in TGF-β1-induced phenotypic transition of mesangial cells by targeting CTNNBIP1. PLoS One 2013; 8(3): e58622.
[81]
Karolina DS, Armugam A, Tavintharan S, et al. MicroRNA 144 impairs insulin signaling by inhibiting the expression of insulin receptor substrate 1 in type 2 diabetes mellitus. PLoS One 2011; 6(8): e22839.
[http://dx.doi.org/10.1371/journal.pone.0022839] [PMID: 21829658]
[82]
Wang Q, Wang Y, Minto AW, et al. MicroRNA‐377 is up‐regulated and can lead to increased fibronectin production in diabetic nephropathy. FASEB J 2008; 22(12): 4126-35.
[http://dx.doi.org/10.1096/fj.08-112326] [PMID: 18716028]
[83]
Chung ACK, Dong Y, Yang W, Zhong X, Li R, Lan HY. Smad7 suppresses renal fibrosis via altering expression of TGF-β/Smad3-regulated microRNAs. Mol Ther 2013; 21(2): 388-98.
[http://dx.doi.org/10.1038/mt.2012.251] [PMID: 23207693]
[84]
Arthur CKC, Xiao RH, Huang R. miR-192 mediates TGF-β/Smad3-driven renal fibrosis. J Am Soc Nephrol 2010; 21(8): 1317-25.
[85]
Deshpande SD, Putta S, Wang M, et al. Transforming growth factor-β-induced cross talk between p53 and a microRNA in the pathogenesis of diabetic nephropathy. Diabetes 2013; 62(9): 3151-62.
[http://dx.doi.org/10.2337/db13-0305] [PMID: 23649518]
[86]
Sumanth P, Linda L, Guangdong S. Inhibiting MicroRNA-192 ameliorates renal fibrosis in diabetic nephropathy. J Am Soc Nephrol 2012; 23(3): 458-69.
[87]
Krupa A, Jenkins R, Luo DD, Lewis A, Phillips A, Fraser D. Loss of MicroRNA-192 promotes fibrogenesis in diabetic nephropathy. J Am Soc Nephrol 2010; 21(3): 438-47.
[http://dx.doi.org/10.1681/ASN.2009050530] [PMID: 20056746]
[88]
Wang B, Komers R, Carew R, et al. Suppression of microRNA-29 expression by TGF-β1 promotes collagen expression and renal fibrosis. J Am Soc Nephrol 2012; 23(2): 252-65.
[http://dx.doi.org/10.1681/ASN.2011010055] [PMID: 22095944]
[89]
Zhong X, Chung ACK, Chen HY, Meng XM, Lan HY. Smad3-mediated upregulation of miR-21 promotes renal fibrosis. J Am Soc Nephrol 2011; 22(9): 1668-81.
[http://dx.doi.org/10.1681/ASN.2010111168] [PMID: 21852586]
[90]
Zhong X, Chung ACK, Chen HY, et al. miR-21 is a key therapeutic target for renal injury in a mouse model of type 2 diabetes. Diabetologia 2013; 56(3): 663-74.
[http://dx.doi.org/10.1007/s00125-012-2804-x] [PMID: 23292313]
[91]
Dey N, Das F, Mariappan MM, et al. MicroRNA-21 orchestrates high glucose-induced signals to TOR complex 1, resulting in renal cell pathology in diabetes. J Biol Chem 2011; 286(29): 25586-603.
[http://dx.doi.org/10.1074/jbc.M110.208066] [PMID: 21613227]
[92]
Wang J, Gao Y, Ma M, et al. Effect of miR-21 on renal fibrosis by regulating MMP-9 and TIMP1 in kk-ay diabetic nephropathy mice. Cell Biochem Biophys 2013; 67(2): 537-46.
[http://dx.doi.org/10.1007/s12013-013-9539-2] [PMID: 23443810]
[93]
Fiorentino L, Cavalera M, Mavilio M, et al. Regulation of TIMP3 in diabetic nephropathy: A role for microRNAs. Acta Diabetol 2013; 50(6): 965-9.
[http://dx.doi.org/10.1007/s00592-013-0492-8] [PMID: 23797704]
[94]
Zhang Z, Peng H, Chen J, et al. MicroRNA-21 protects from mesangial cell proliferation induced by diabetic nephropathy in db/db mice. FEBS Lett 2009; 583(12): 2009-14.
[http://dx.doi.org/10.1016/j.febslet.2009.05.021] [PMID: 19450585]
[95]
Ding Q, Gladson CL, Wu H, Hayasaka H, Olman MA. Focal adhesion kinase (FAK)-related non-kinase inhibits myofibroblast differentiation through differential MAPK activation in a FAK-dependent manner. J Biol Chem 2008; 283(40): 26839-49.
[http://dx.doi.org/10.1074/jbc.M803645200] [PMID: 18669633]
[96]
Roy S, Khanna S, Hussain SRA, et al. MicroRNA expression in response to murine myocardial infarction: miR-21 regulates fibroblast metalloprotease-2 via phosphatase and tensin homologue. Cardiovasc Res 2009; 82(1): 21-9.
[http://dx.doi.org/10.1093/cvr/cvp015] [PMID: 19147652]
[97]
Thum T, Gross C, Fiedler J, et al. MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts. Nature 2008; 456(7224): 980-4.
[http://dx.doi.org/10.1038/nature07511] [PMID: 19043405]
[98]
Kriegel AJ, Liu Y, Fang Y, Ding X, Liang M. The miR-29 family: Genomics, cell biology, and relevance to renal and cardiovascular injury. Physiol Genomics 2012; 44(4): 237-44.
[http://dx.doi.org/10.1152/physiolgenomics.00141.2011] [PMID: 22214600]
[99]
Qin W, Chung ACK, Huang XR, et al. TGF-β/Smad3 signaling promotes renal fibrosis by inhibiting miR-29. J Am Soc Nephrol 2011; 22(8): 1462-74.
[http://dx.doi.org/10.1681/ASN.2010121308] [PMID: 21784902]
[100]
van Rooij E, Sutherland LB, Thatcher JE, et al. Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis. Proc Natl Acad Sci 2008; 105(35): 13027-32.
[http://dx.doi.org/10.1073/pnas.0805038105] [PMID: 18723672]
[101]
Xiao J, Meng XM, Huang XR, et al. miR-29 inhibits bleomycin-induced pulmonary fibrosis in mice. Mol Ther 2012; 20(6): 1251-60.
[http://dx.doi.org/10.1038/mt.2012.36] [PMID: 22395530]
[102]
Du B, Ma LM, Huang MB, et al. High glucose down-regulates miR-29a to increase collagen IV production in HK-2 cells. FEBS Lett 2010; 584(4): 811-6.
[http://dx.doi.org/10.1016/j.febslet.2009.12.053] [PMID: 20067797]
[103]
Du T, Zamore PD. microPrimer: The biogenesis and function of microRNA. Development 2005; 132(21): 4645-52.
[http://dx.doi.org/10.1242/dev.02070] [PMID: 16224044]
[104]
Liu Y, Taylor NE, Lu L, et al. Renal medullary microRNAs in Dahl salt-sensitive rats: miR-29b regulates several collagens and related genes. Hypertension 2010; 55(4): 974-82.
[http://dx.doi.org/10.1161/HYPERTENSIONAHA.109.144428] [PMID: 20194304]
[105]
Ye Y, Hu Z, Lin Y, Zhang C, Perez-Polo JR. Downregulation of microRNA-29 by antisense inhibitors and a PPAR-γ agonist protects against myocardial ischaemia-reperfusion injury. Cardiovasc Res 2010; 87(3): 535-44.
[http://dx.doi.org/10.1093/cvr/cvq053] [PMID: 20164119]
[106]
Howe EN, Cochrane DR, Richer JK. The miR-200 and miR-221/222 microRNA Families: Opposing effects on epithelial identity. J Mammary Gland Biol Neoplasia 2012; 17(1): 65-77.
[http://dx.doi.org/10.1007/s10911-012-9244-6] [PMID: 22350980]
[107]
Gregory PA, Bert AG, Paterson EL, et al. The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1. Nat Cell Biol 2008; 10(5): 593-601.
[http://dx.doi.org/10.1038/ncb1722] [PMID: 18376396]
[108]
Korpal M, Lee ES, Hu G, Kang Y. The miR-200 family inhibits epithelial-mesenchymal transition and cancer cell migration by direct targeting of E-cadherin transcriptional repressors ZEB1 and ZEB2. J Biol Chem 2008; 283(22): 14910-4.
[http://dx.doi.org/10.1074/jbc.C800074200] [PMID: 18411277]
[109]
Park SM, Gaur AB, Lengyel E, Peter ME. The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2. Genes Dev 2008; 22(7): 894-907.
[http://dx.doi.org/10.1101/gad.1640608] [PMID: 18381893]
[110]
Burk U, Schubert J, Wellner U, et al. A reciprocal repression between ZEB1 and members of the miR‐200 family promotes EMT and invasion in cancer cells. EMBO Rep 2008; 9(6): 582-9.
[http://dx.doi.org/10.1038/embor.2008.74] [PMID: 18483486]
[111]
Wang B, Koh P, Winbanks C, et al. miR-200a Prevents renal fibrogenesis through repression of TGF-β2 expression. Diabetes 2011; 60(1): 280-7.
[http://dx.doi.org/10.2337/db10-0892] [PMID: 20952520]
[112]
Xiong M, Jiang L, Zhou Y, et al. The miR-200 family regulates TGF-β1-induced renal tubular epithelial to mesenchymal transition through Smad pathway by targeting ZEB1 and ZEB2 expression. Am J Physiol Renal Physiol 2012; 302(3): F369-79.
[http://dx.doi.org/10.1152/ajprenal.00268.2011] [PMID: 22012804]
[113]
Wang G, Kwan BCH, Lai FMM, Chow KM, Li PKT, Szeto CC. Urinary miR-21, miR-29, and miR-93: Novel biomarkers of fibrosis. Am J Nephrol 2012; 36(5): 412-8.
[http://dx.doi.org/10.1159/000343452] [PMID: 23108026]
[114]
Conserva F, Barozzino M, Pesce F, et al. Urinary miRNA-27b-3p and miRNA-1228-3p correlate with the progression of Kidney Fibrosis in Diabetic Nephropathy. Sci Rep 2019; 9(1): 11357.
[http://dx.doi.org/10.1038/s41598-019-47778-1] [PMID: 31388051]
[115]
Zhou LT, Qiu S, Lv LL, et al. Integrative bioinformatics analysis provides insight into the molecular mechanisms of chronic kidney disease. Kidney Blood Press Res 2018; 43(2): 568-81.
[http://dx.doi.org/10.1159/000488830] [PMID: 29642064]
[116]
Zhong M, Wu Y, Ou W, Huang L, Yang L. Identification of key genes involved in type 2 diabetic islet dysfunction: A bioinformatics study. Biosci Rep 2019; 39(5): BSR20182172.
[http://dx.doi.org/10.1042/BSR20182172] [PMID: 31088900]
[117]
Shu B, Fang Y, He W, Yang J, Dai C. Identification of macrophage-related candidate genes in lupus nephritis using bioinformatics analysis. Cell Signal 2018; 46: 43-51.
[http://dx.doi.org/10.1016/j.cellsig.2018.02.006] [PMID: 29458096]
[118]
Butz H, Szabó PM, Nofech-Mozes R, et al. Integrative bioinformatics analysis reveals new prognostic biomarkers of clear cell renal cell carcinoma. Clin Chem 2014; 60(10): 1314-26.
[http://dx.doi.org/10.1373/clinchem.2014.225854] [PMID: 25139457]
[119]
Wang WN, Zhang WL, Zhou GY, et al. Prediction of the molecular mechanisms and potential therapeutic targets for diabetic nephropathy by bioinformatics methods. Int J Mol Med 2016; 37(5): 1181-8.
[http://dx.doi.org/10.3892/ijmm.2016.2527] [PMID: 26986014]
[120]
Martinez-Moreno JM, Fontecha-Barriuso M, Martin-Sanchez D, et al. Epigenetic modifiers as potential therapeutic targets in diabetic kidney disease. Int J Mol Sci 2020; 21(11): 4113.
[http://dx.doi.org/10.3390/ijms21114113] [PMID: 32526941]
[121]
Epigenetic modifications in the pathogenesis of diabetic nephropathy. Semin Nephrol 2013; 33: 341-53.
[http://dx.doi.org/10.1016/j.semnephrol.2013.05.006] [PMID: 24011576]
[122]
Thomas MC. Epigenetic mechanisms in diabetic Kidney Disease. Curr Diab Rep 2016; 16(3): 31.
[http://dx.doi.org/10.1007/s11892-016-0723-9] [PMID: 26908156]
[123]
Shao K, Shen LS, Li HH, Huang S, Zhang Y. Systematic‐analysis of mRNA expression profiles in skeletal muscle of patients with type II diabetes: The glucocorticoid was central in pathogenesis. J Cell Physiol 2018; 233(5): 4068-76.
[http://dx.doi.org/10.1002/jcp.26174] [PMID: 28885689]
[124]
Cui Z, Zeng Q, Guo Y. Integrated bioinformatic changes and analysis of retina with time in diabetic rats. PeerJ 2018; 6: e4762.
[125]
Pinzón-Cortés JA, Perna-Chaux A, Rojas-Villamizar NS. Effect of diabetes status and hyperglycemia on global DNA methylation and hydroxymethylation. Endocr Connect 2017; 6(8): 708-25.
[126]
Cubillos-Angulo JM, Vinhaes CL, Fukutani ER. In silico transcriptional analysis of mRNA and miRNA reveals unique biosignatures that characterizes different types of diabetes. PLoS One 2020; 15(9): e0239061.
[127]
Wang Z, Wang Z, Zhou Z, Ren Y. Crucial genes associated with diabetic nephropathy explored by microarray analysis. BMC Nephrol 2016; 17(1): 128.
[http://dx.doi.org/10.1186/s12882-016-0343-2] [PMID: 27613243]
[128]
Rai B, Kumar Maurya P, Srivastava M, Mishra P, Hasan Asif M, Tiwari S. An in-silico approach to identify therapeutic target and markers associated with diabetic nephropathy. Curr Diabetes Rev 2022; 19.
[http://dx.doi.org/10.2174/1573399819666220610191935] [PMID: 35702773]
[129]
Yang H, Lian D, Zhang X, Li H, Xin G. Key genes and signaling pathways contribute to the pathogensis of diabetic nephropathy. Iran J Kidney Dis 2019; 13(2): 87-97.
[PMID: 30988245]
[130]
Motshwari D, Matshazi D, Erasmus R, Kengne A, Matsha T, George C. MicroRNAs associated with chronic kidney disease in the general population and high-risk subgroups—a systematic review. Int J Mol Sci 2023; 24(2): 1792.
[http://dx.doi.org/10.3390/ijms24021792] [PMID: 36675311]
[131]
Le-Ting Z, Lin-Li LV, Shen Q. Bioinformatics-based discovery of the urinary BBOX1 mRNA as a potential biomarker of diabetic kidney disease. J Transl Med 2019; 17: 59.
[132]
Taís SA, Recamonde-Mendoza M, Aline RC. Circulating miRNAs in diabetic kidney disease: Case-control study and in silico analyses. Acta Diabetol 2019; 56(1): 55-65.
[133]
Hou YP, Diao TT, Xu ZH, Mao XY, Wang C, Li B. Bioinformatic analysis combined with experimental validation reveals novel hub genes and pathways associated with focal segmental glomerulosclerosis. Front Mol Biosci 2022; 8: 691966.
[http://dx.doi.org/10.3389/fmolb.2021.691966] [PMID: 35059432]
[134]
Assmann TS, Recamonde-Mendoza M, de Souza BM, Bauer AC, Crispim D. MicroRNAs and diabetic kidney disease: Systematic review and bioinformatic analysis. Mol Cell Endocrinol 2018; 477: 90-102.
[http://dx.doi.org/10.1016/j.mce.2018.06.005] [PMID: 29902497]

Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy