Advances in role of miR-296 in fibrosis-related diseases

Abstract

Abstract: The fibrosis is an excessive repair response of the organism,which can lead to a variety of tissue and organ dysfunctions manifested by fibroblast activation,proliferation and excessive deposition of extracellular matrix. The microRNA（miRNA） is not only directly involved in the process of multi-organ fibrosis,but also the expression level is affected by the degree of fibrosis,which is a key regulatory factor. In recent years,miR-296 has been found to be dysregulated in fibrosis-related diseases,targets genes involved in fibrosis signaling pathways such as TGF-β and JAK2/STAT3,inflammatory response,cell apoptosis,autophagy,collagen synthesis,and capillary injury through targeted regulation,fibroblast proliferation,epithelial mesenchymal transition,synthesis and degradation of extracellular matrix,and regulates fibrosis process. The paper reviews the mechanism of miR-296's involvement in fibrosis-associated diseases and its potential in the diagnosis and treatment of fibrosis-associated diseases.

Key words: miR-296, Fibrosis-related diseases, Mechanism of action, Review

CLC Number:

R181.3

WANG Chenyu, YE Lifang, LIU Su. Advances in role of miR-296 in fibrosis-related diseases. [J]OCCUPATION AND HEALTH, 2025, 41(3): 420-424.

References

[1] 韩敏,聂静,李萃,等.脏器纤维化的研究进展和重要科学问题[J].中国病理生理杂志,2018,34(8):1518-1526.
[2] WYNN T A,RAMALINGAM T R.Mechanisms of fibro-sis:Therapeutic translation for fibrotic disease[J].Nat Med,2012,18(7):1028-1240.
[3] ANDREOU I,SUN X,STONE P H,et al.miRNAs in atherosclerotic plaque initiation,progression,and rupture[J].Trends Mol Med,2015, 21(5):307-318.
[4] BARTEL D P.MicroRNAs:Genomics,biogenesis,mechanism,and function[J].Cell,2004,116(2):281-297.
[5] JIANG X,TSITSIOU E,HERRICK S E,et al.MicroRNAs and the regulation of fibrosis[J].FEBS J,2010,277(9):2015-2021.
[6] SCHNAPER H W,KOPP J B.Renal fibrosis[J].Front Biosci,2003,8:e68-e86.
[7] 叶泽华,夏煜琦,程帆.miRNA和lncRNA在肾纤维化中作用的研究进展[J].中华实用诊断与治疗杂志,2022,36(11):1185-1188.
[8] NI W J,TANG L Q,WEI W.Research progress in signalling pathway in diabetic nephropathy[J].Diabetes Metab Res Rev,2015,31(3):221-233.
[9] ZHANG W,ZHANG S.Downregulation of circRNA-0000285 suppresses cervical cancer development by regulating miR197-3p-ELK1 Axis[J].Cancer Manag Res,2020,12:8663-8674.
[10] XIONG D D,DANG Y W,LIN P,et al.A circRNA-miRNA-mRNA network identification for exploring underlying pathogenesis and therapy strategy of hepatocellular carcinoma[J].J Transl Med,2018,16(1):220.
[11] TANG B,LI W,JI T T,et al.Circ-AKT3 inhibits theaccumulation of extracellular matrix of mesangial cells in diabetic nephropathy via modulating miR-296-3p/E-cadherin signals[J].J Cell Mol Med,2020, 24(15):8779-8788.
[12] ZEISBERG E M,POTENTA S E,SUGIMOTO H,et al.Fibroblasts in kidney fibrosis emerge via endothelial-to-mesenchymal transition[J]. J Am Soc Nephrol,2008,19(12):2282-2287.
[13] VILLAREJO A,CORTÉS-CABRERA A,MOLINA-ORTÍZ P,et al. Differential role of Snail1 and Snail2 zinc fingers in E-cadherin repression and epithelial to mesenchymal transition[J].J Biol Chem,2014,289(2):930-941.
[14] WANG Y,LIU Y,ZHANG L,et al.miR-30b-5p modulate renal epithelial-mesenchymal transition in diabeticnephropathy by directly targeting SNAI1[J].Biochem Biophys Res Commun,2021,535:12-18.
[15] 刘苏,徐巍龙,查敏,等.miR-296-5p在糖尿病肾病db/db小鼠血浆外泌体中的表达及功能[J].南京医科大学学报(自然科学版),2022, 42(1):14-22.
[16] CHEN F,XIE Y,LV Q,et al.Curcumin mediates repulsive guidance molecule B(RGMb) in the treatment mechanism of renal fibrosis induced by unilateral ureteral obstruction[J].Ren Fail,2021,43(1):1496-1505.
[17] MAEDA S,MATSUI T,TAKEUCHI M,et al.Sodiumglucose cotransporter 2-mediated oxidative stress augments advanced glycation end products-induced tubular cell apoptosis[J].Diabetes Metab Res Rev,2013,29(5):406-412.
[18] CHEN S.circ_000166/miR-296 Aggravates the process of diabetic renal fibrosis by regulating the SGLT2 signaling pathway in renal tubular epithelial cells[J].Dis Markers,2022,2022:6103086.
[19] KANG D H,ANDERSON S,KIM Y G,et al.Impaired angiogenesis in the aging kidney:Vascular endothelial growth factor and thrombospondin-1 in renal disease[J].Am J Kidney Dis,2001,37(3):601-611.
[20] LI S,WANG F,SUN D.The renal microcirculation in chronic kidney disease:Novel diagnostic methods and therapeutic perspectives[J].Cell Biosci,2021,11(1):90.
[21] CHEVALIER R L,FORBES M S,THORNHILL B A.Ureteral obstruction as a model of renal interstitial fibrosis and obstructive nephropathy[J].Kidney Int,2009,75(11):1145-1152.
[22] BORGES F T,MELO S A,ÖZDEMIR B C,et al.TGF-β1-containing exosomes from injured epithelial cells activate fibroblasts to initiate tissue regenerative responses and fibrosis[J].J Am Soc Nephrol,2013, 24(3):385-392.
[23] GRANGE C,SKOVRONOVA R,MARABESE F,et al.Stem cell-derived extracellular vesicles and kidney regeneration[J].Cells,2019,8(10):1240.
[24] SAHOO S,KLYCHKO E,THORNE T,et al.Exosomes from human CD34(+) stem cells mediate their proangiogenic paracrine activity[J] Circ Res,2011,109(7):724-728.
[25] CANTALUPPI V,GATTI S,MEDICA D,et al.Microvesicles derived from endothelial progenitor cells protect the kidney from ischemia-reperfusion injury by microRNA-dependent reprogramming of resident renal cells[J].Kidney Int,2012,82(4):412-427.
[26] KAPITSINOU P P,JAFFE J,MICHAEL M,et al.Preischemic targeting of HIF prolyl hydroxylation inhibits fibrosis associated with acute kidney injury[J].Am J Physiol Renal Physiol,2012,302(9):1172-1179.
[27] ROEHLEN N,CROUCHET E,BAUMERT T F.Liver fibrosis:Mechanistic concepts and therapeutic perspectives[J].Cells,2020,9(4):875.
[28] HE Y,HUANG C,LIN X,et al.MicroRNA-29 family,a crucial therapeutic target for fibrosis diseases[J].Biochimie,2013,95(7):1355-1359.
[29] HIGASHI T,FRIEDMAN S L,HOSHIDA Y.Hepatic stellate cells as key target in liver fibrosis[J].Adv Drug Deliv Rev,2017:121127-121142.
[30] TSUCHIDA T,FRIEDMAN S L.Mechanisms of hepatic stellate cell activation[J].Nat Rev Gastroenterol Hepatol,2017,14(7):397-411.
[31] EZHILARASAN D.MicroRNA interplay between hepatic stellate cell quiescence and activation[J].Eur J Pharmacol,2020,885:173507.
[32] ZHANGDI H J,SU S B,WANG F,et al.Crosstalk network among multiple inflammatory mediators in liver fibrosis[J].World J Gastroenterol,2019,25(33):4835-4849.
[33] TSAI Y S,YEH M L,TSAI P C,et al.Clusters of Circulating let-7 family tumor suppressors are associated with clinical characteristics of chronic hepatitis C[J].Int J Mol Sci,2020,21(14):4945.
[34] TAVAKOLI DARGANI Z,SINGLA D K.Embryonic stem cell-derived exosomes inhibit doxorubicin-induced TLR4-NLRP3-mediated cell death-pyroptosis[J].Am J Physiol Heart Circ Physiol,2019,317(2):H460-H471.
[35] 马艳珍. CircAno6/miR-296-3p/TLR4信号轴介导炎症级联反应诱导HSCs活化的机制及疏肝健脾方的干预研究[D].合肥:安徽中医药大学,2023.
[36] LEE S J,KIM K H,PARK K K.Mechanisms of fibrogenesis in liver cirrhosis:The molecular aspects of epithelial-mesenchymal transition[J].World J Hepatol,2014,6(4):207-216.
[37] SHAKERI H,BOEN J R A,DE MOUDT S,et al.Neuregulin-1 compensates for endothelial nitric oxide synthase deficiency[J].Am J Physiol Heart Circ Physiol,2021,320,H2416-H2428.
[38] SHI D M,SHI X L,XING K L,et al.miR-296-5p suppresses stem cell potency of hepatocellular carcinoma cells via regulating Brg1/Sall4 axis[J].Cell Signal,2020,72:109650.
[39] 张靖,左雁,李振宇,等.miRNA调控肺纤维化信号通路TGF-β的研究进展[J].世界最新医学信息文摘,2016,16(A2):32-33,35.
[40] LIU H,CHENG Y,YANG J,et al.BBC3 in macrophages promoted pulmonary fibrosis development through inducing autophagy during silicosis[J].Cell Death Dis,2017,8(3):e2657.
[41] WU Q,JIAO B,ZHANG Q,et al.Identification of circRNA expression profiles and the potential role of hsa_circ_0006916 in silicosis and pulmonary fibrosis[J].Toxicology,2023,483:153384.
[42] SOLIMAN H,ROSSI F M V.Cardiac fibroblast diversity in health and disease[J].Matrix Biol,2020,91-92:75-91.
[43] LIN R,RAHTU-KORPELA L,SZABO Z,et al.MiR-185-5p regulates the development of myocardial fibrosis[J].J Mol Cell Cardiol,2022, 165:130-140.
[44] WEBER K T,SUN Y,BHATTACHARYA S K,et al.Myofibroblast-mediated mechanisms of pathological remodelling of the heart[J].Nat Rev Cardiol,2013,10(1):15-26.
[45] YIN Z,GUO Y,ZHANG J,et al.Association between an indel polymorphism in the 3'UTR of COL1A2 and the risk of sudden cardiac death in Chinese populations[J].Leg Med(Tokyo),2017,28:22-26.
[46] VIENBERG S,GEIGER J,MADSEN S,et al.MicroRNAs in metabo-
lism[J].Acta Physiol(Oxf),2017,219(2):346-361.
[47] FANG L,ELLIMS A H,MOORE X L,et al.Circulating microRNAs as biomarkers for diffuse myocardial fibrosis in patients with hypertrophic cardiomyopathy[J].J Transl Med,2015,13:314.
[48] ZHANG T,WANG X F,WANG Z C,et al.Current potential therapeutic strategies targeting the TGF-β/Smad signaling pathway to attenuate keloid and hypertrophic scar formation[J].Biomed Pharmacother,2020,129:110287.
[49] 郭冰玉,林枫,白泽明,等.微小RNA-296在兔增生性瘢痕中的表达及对人成纤维细胞的作用[J].中华烧伤杂志,2021,37(8):725-730.
[50] ZHANG X W,WANG L,DING H.Long noncoding RNA AK089579 inhibits epithelial-to-mesenchymal transition of peritoneal mesothelial cells by competitively binding to microRNA-296-3p via DOK2 in peritonealfibrosis[J].FASEB J,2019,33(4):5112-5125.