Research progress in the role of non-coding RNA in regulating pancreatic fibrosis

doi:10.3877/cma.j.issn.2095-3232.2024.04.024

Abstract

Abstract:

Pancreatic fibrosis (PF) is a pathological process of pancreatic tissue damage and repair caused by multiple pathogenic factors. The pathological characteristics mainly include excessive deposition of extracellular matrix (ECM) components in the pancreas caused by recurrent inflammation and necrosis. The incidence and development of PF are intimately associated with multiple diseases such as chronic pancreatitis, pancreatic cancer and pancreatic cystic fibrosis, etc. The activation, synthesis and secretion of a large quantity of ECM components by pancreatic stellate cells (PSCs) are the core events throughout the process of PF. Recent studies have shown that non-coding RNA (ncRNA) plays an important role in the development of PF. Clarifying the mechanism of ncRNA in the process of PF contributes to unraveling the mechanism of PF and providing basis for rational treatment. Therefore, the mechanism underlying the role of ncRNA in PF was illustrated.

Key words: Pancreatic fibrosis, Pancreatic stellate cells, Non-coding RNA (ncRNA)

Hang Zhai, Guangquan Zhang, Fangfang Wu, Xianjie Shi. Research progress in the role of non-coding RNA in regulating pancreatic fibrosis[J]. Chinese Journal of Hepatic Surgery(Electronic Edition), 2024, 13(04): 583-587.

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References 48

[1]	Ceyhan GO, Friess H. Pancreatic disease in 2014: pancreatic fibrosis and standard diagnostics[J]. Nat Rev Gastroenterol Hepatol, 2015, 12(2):68-70.
[2]	Yang X, Chen J, Wang J, et al. Very-low-density lipoprotein receptor-enhanced lipid metabolism in pancreatic stellate cells promotes pancreatic fibrosis[J]. Immunity, 2022, 55(7):1185-1199, e8.
[3]	Jiang W, Jin L, Ju D, et al. The pancreatic clock is a key determinant of pancreatic fibrosis progression and exocrine dysfunction[J]. Sci Transl Med, 2022, 14(664):eabn3586.
[4]	Matsui M, Corey DR. Non-coding RNAs as drug targets[J]. Nat Rev Drug Discov, 2017, 16(3):167-179.
[5]	Zhang T, Zhang G, Yang W, et al. Lnc-PFAR facilitates autophagy and exacerbates pancreatic fibrosis by reducing pre-miR-141 maturation in chronic pancreatitis[J]. Cell Death Dis, 2021, 12(11): 996.
[6]	Dey S, Udari LM, RiveraHernandez P, et al. Loss of miR-29a/b1 promotes inflammation and fibrosis in acute pancreatitis[J]. JCI Insight, 2021, 6(19):e149539.
[7]	Ye J, Lin Y, Yu Y, et al. LncRNA NEAT1/microRNA-129-5p/SOCS2 axis regulates liver fibrosis in alcoholic steatohepatitis[J]. J Transl Med, 2020, 18(1):445.
[8]	Apte MV, Haber PS, Applegate TL, et al. Periacinar stellate shaped cells in rat pancreas: identification, isolation, and culture[J]. Gut, 1998, 43(1):128-133.
[9]	Yan Z, Ohuchida K, Fei S, et al. Inhibition of ERK1/2 in cancer-associated pancreatic stellate cells suppresses cancer-stromal interaction and metastasis[J]. J Exp Clin Cancer Res, 2019, 38(1): 221.
[10]	Auwercx J, Kischel P, Lefebvre T, et al. TRPM7 modulates human pancreatic stellate cell activation[J]. Cells, 2022, 11(14):2255.
[11]	Zhang Y, Ware MB, Zaidi MY, et al. Heat shock protein-90 inhibition alters activation of pancreatic stellate cells and enhances the efficacy of PD-1 blockade in pancreatic cancer[J]. Mol Cancer Ther, 2021, 20(1):150-160.
[12]	Yao W, Luo D, Lv Z, et al. The Rabep1-mediated endocytosis and activation of trypsinogen to promote pancreatic stellate cell activation[J]. Biomolecules, 2022, 12(8):1063.
[13]	Lee JH, Massagué J. TGF-β in developmental and fibrogenic EMTs[J]. Semin Cancer Biol, 2022, 86(Pt 2):136-145.
[14]	Jaster R, Sparmann G, Emmrich J, et al. Extracellular signal regulated kinases are key mediators of mitogenic signals in rat pancreatic stellate cells[J]. Gut, 2002, 51(4):579-584.
[15]	Humeres C, Shinde AV, Hanna A, et al. Smad7 effects on TGF-β and ErbB2 restrain myofibroblast activation and protect from postinfarction heart failure[J]. J Clin Invest, 2022, 132(3):e146926.
[16]	Dooley S, Hamzavi J, Breitkopf K, et al. Smad7 prevents activation of hepatic stellate cells and liver fibrosis in rats[J]. Gastroenterology, 2003, 125(1):178-191.
[17]	Ghafouri-Fard S, Abak A, Talebi SF, et al. Role of miRNA and lncRNAs in organ fibrosis and aging[J]. Biomedecine Pharmacother, 2021, 143:112132.
[18]	Wang X, He Y, Mackowiak B, et al. MicroRNAs as regulators, biomarkers and therapeutic targets in liver diseases[J]. Gut, 2021, 70(4):784-795.
[19]	Yang Z, Jiang S, Shang J, et al. LncRNA: shedding light on mechanisms and opportunities in fibrosis and aging[J]. Ageing Res Rev, 2019, 52:17-31.
[20]	Rupaimoole R, Slack FJ. MicroRNA therapeutics: towards a new era for the management of cancer and other diseases[J]. Nat Rev Drug Discov, 2017, 16(3):203-222.
[21]	Krol J, Loedige I, Filipowicz W. The widespread regulation of microRNA biogenesis, function and decay[J]. Nat Rev Genet, 2010, 11(9):597-610.
[22]	Iorio MV, Croce CM. MicroRNA dysregulation in cancer: diagnostics, monitoring and therapeutics. a comprehensive review[J]. EMBO Mol Med, 2017, 9(6):852.
[23]	Dong J, Huth WJ, Marcel N, et al. MiR-15/16 clusters restrict effector Treg cell differentiation and function[J]. J Exp Med, 2023, 220(10):e20230321.
[24]	Tijsen AJ, van der Made I, van den Hoogenhof MM, et al. The microRNA-15 family inhibits the TGFβ-pathway in the heart[J]. Cardiovasc Res, 2014, 104(1):61-71.
[25]	Rawal S, Munasinghe PE, Nagesh PT, et al. Down-regulation of miR-15a/b accelerates fibrotic remodelling in the type 2 diabetic human and mouse heart[J]. Clin Sci, 2017, 131(9):847-863.
[26]	Ji T, Feng W, Zhang X, et al. HDAC inhibitors promote pancreatic stellate cell apoptosis and relieve pancreatic fibrosis by upregulating miR-15/16 in chronic pancreatitis[J]. Hum Cell, 2020, 33(4):1006-1016.
[27]	Yang S, Banerjee S, de Freitas A, et al. Participation of miR-200 in pulmonary fibrosis[J]. Am J Pathol, 2012, 180(2):484-493.
[28]	Sundararajan V, Burk UC, Bajdak-Rusinek K. Revisiting the miR-200 family: a clan of five siblings with essential roles in development and disease[J]. Biomolecules, 2022, 12(6):781.
[29]	Hussein RM, Anwar MM, Farghaly HS, et al. Gallic acid and ferulic acid protect the liver from thioacetamide-induced fibrosis in rats via differential expression of miR-21, miR-30 and miR-200 and impact on TGF-β1/Smad3 signaling[J]. Chem Biol Interact, 2020, 324: 109098.
[30]	Mansour SM, El-Abhar HS, Soubh AA. MiR-200a inversely correlates with Hedgehog and TGF-β canonical/non-canonical trajectories to orchestrate the anti-fibrotic effect of Tadalafil in a bleomycin-induced pulmonary fibrosis model[J]. Inflammopharmacology, 2021, 29(1):167-182.
[31]	Wang Y, Zeng Z, Guan L, et al. GRHL2 induces liver fibrosis and intestinal mucosal barrier dysfunction in non-alcoholic fatty liver disease via microRNA-200 and the MAPK pathway[J]. J Cell Mol Med, 2020, 24(11):6107-6119.
[32]	Xu M, Wang G, Zhou H, et al. TGF-β1-miR-200a-PTEN induces epithelial-mesenchymal transition and fibrosis of pancreatic stellate cells[J]. Mol Cell Biochem, 2017, 431(1/2):161-168.
[33]	Wang Y, Du J, Niu X, et al. MiR-130a-3p attenuates activation and induces apoptosis of hepatic stellate cells in nonalcoholic fibrosing steatohepatitis by directly targeting TGFBR1 and TGFBR2[J]. Cell Death Dis, 2017, 8(5):e2792.
[34]	Ai K, Zhu X, Kang Y, et al. MiR-130a-3p inhibition protects against renal fibrosis in vitro via the TGF-β1/Smad pathway by targeting SnoN[J]. Exp Mol Pathol, 2020, 112:104358.
[35]	Ding Y, Hou Y, Liu Y, et al. MiR-130a-3p alleviates inflammatory and fibrotic phases of pulmonary fibrosis through proinflammatory factor TNF-α and profibrogenic receptor TGF-βRII[J]. Front Pharmacol, 2022, 13:863646.
[36]	Wang Q, Wang H, Jing Q, et al. Regulation of pancreatic fibrosis by acinar cell-derived exosomal miR-130a-3p via targeting of stellate cell PPAR-Γ[J]. J Inflamm Res, 2021, 14:461-477.
[37]	Nojima T, Proudfoot NJ. Mechanisms of lncRNA biogenesis as revealed by nascent transcriptomics[J]. Nat Rev Mol Cell Biol, 2022, 23(6):389-406.
[38]	Kopp F, Mendell JT. Functional classification and experimental dissection of long noncoding RNAs[J]. Cell, 2018, 172(3):393-407.
[39]	Tan YT, Lin JF, Li T, et al. LncRNA-mediated posttranslational modifications and reprogramming of energy metabolism in cancer[J]. Cancer Commun, 2021, 41(2):109-120.
[40]	Zhu J, Fu H, Wu Y, et al. Function of lncRNAs and approaches to lncRNA-protein interactions[J]. Sci China Life Sci, 2013, 56(10): 876-885.
[41]	Bridges MC, Daulagala AC, Kourtidis A. LNCcation: lncRNA localization and function[J]. J Cell Biol, 2021, 220(2):e202009045.
[42]	Yang L, Deng J, Ma W, et al. Ablation of lncRNA Miat attenuates pathological hypertrophy and heart failure[J]. Theranostics, 2021, 11(16):7995-8007.
[43]	Chen Y, Chen X, Li H, et al. Serum extracellular vesicles containing MIAT induces atrial fibrosis, inflammation and oxidative stress to promote atrial remodeling and atrial fibrillation via blockade of miR-485-5p-mediated CXCL10 inhibition[J]. Clin Transl Med, 2021, 11(8):e482.
[44]	Zhan Y, Tao Q, Meng Q, et al. LncRNA-MIAT activates hepatic stellate cells via regulating Hippo pathway and epithelial-to-mesenchymal transition[J]. Commun Biol, 2023, 6(1):285.
[45]	Bijkerk R, Au YW, Stam W, et al. Long non-coding RNAs rian and miat mediate myofibroblast formation in kidney fibrosis[J]. Front Pharmacol, 2019, 10:215.
[46]	Xiao W, Zheng D, Chen X, et al. Long non-coding RNA MIAT is involved in the regulation of pyroptosis in diabetic cardiomyopathy via targeting miR-214-3p[J]. iScience, 2021, 24(12):103518.
[47]	Liu H, Yu K, Ma P, et al. Long noncoding RNA myocardial infarction-associated transcript regulated the pancreatic stellate cell activation to promote the fibrosis process of chronic pancreatitis[J].J Cell Biochem, 2019, 120(6):9547-9555.
[48]	Zhao X, Sun J, Chen Y, et al. lncRNA PFAR promotes lung fibroblast activation and fibrosis by targeting miR-138 to regulate the YAP1-twist axis[J]. Mol Ther, 2018, 26(9):2206-2217.

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