205
Views
0
CrossRef citations to date
0
Altmetric
Review

Exosomal microRNAs: Potential Nanotherapeutic Targets for Diabetic Kidney Disease

, & ORCID Icon
Pages 1669-1680 | Received 29 Jan 2023, Accepted 05 Sep 2023, Published online: 01 Nov 2023

References

  • Zhao L , ZhangJ, LeiSet al. Combining glomerular basement membrane and tubular basement membrane assessment improves the prediction of diabetic end-stage renal disease. J. Diabetes13(7), 572–584 (2021).
  • Sugita E , HayashiK, HishikawaA, ItohH. Epigenetic alterations in podocytes in diabetic nephropathy. Front. Pharmacol.12, 759299 (2021).
  • Das F , BeraA, Ghosh-ChoudhuryNet al. High glucose-stimulated enhancer of zeste homolog-2 (EZH2) forces suppression of deptor to cause glomerular mesangial cell pathology. Cell. Signal.86, 110072 (2021).
  • Vallon V , ThomsonSC. Renal function in diabetic disease models: the tubular system in the pathophysiology of the diabetic kidney. Annu. Rev. Physiol.74, 351–375 (2012).
  • Vartak T , GodsonC, BrennanE. Therapeutic potential of pro-resolving mediators in diabetic kidney disease. Adv. Drug Deliv. Rev.178, 113965 (2021).
  • Thethi T , KamiyamaM, KoboriH. The link between the renin–angiotensin–aldosterone system and renal injury in obesity and the metabolic syndrome. Curr. Hypertens. Rep.14(2), 160–169 (2012).
  • Magee C , GrieveDJ, WatsonCJ, BrazilDP. Diabetic nephropathy: a tangled web to unweave. Cardiovasc. Drugs Ther.31(5–6), 579–592 (2017).
  • Jung SW , MoonJY. The role of inflammation in diabetic kidney disease. Korean J. Int. Med.36(4), 753–766 (2021).
  • Samsu N . Diabetic nephropathy: challenges in pathogenesis, diagnosis, and treatment. Biomed. Res. Int.2021, 1497449 (2021).
  • Lassén E , DaehnIS. Molecular mechanisms in early diabetic kidney disease: glomerular endothelial cell dysfunction. Int. J. Mol. Sci.21(24), 9456 (2020).
  • Nishad R , TahaseenV, KavvuriRet al. Advanced-glycation end-products induce podocyte injury and contribute to proteinuria. Front. Med.8, 685447 (2021).
  • Zhang PN , ZhouMQ, GuoJet al. Mitochondrial dysfunction and diabetic nephropathy: nontraditional therapeutic opportunities. J. Diabetes Res.2021, 1010268 (2021).
  • Mostafa DK , KhedrMM, BarakatMK, AbdellatifAA, ElsharkawyAM. Autophagy blockade mechanistically links proton pump inhibitors to worsened diabetic nephropathy and aborts the renoprotection of metformin/enalapril. Life Sci.265, 118818 (2021).
  • Kalluri R , LeBleuVS. The biology, function, and biomedical applications of exosomes. Science367(6478), eaau6977 (2020).
  • He X , KuangG, WuY, OuC. Emerging roles of exosomal miRNAs in diabetes mellitus. Clin. Transl. Med.11(6), e468 (2021).
  • Colombo M , RaposoG, ThéryC. Biogenesis, secretion, and intercellular interactions of exosomes and other extracellular vesicles. Ann. Rev. Cell Dev. Biol.30, 255–289 (2014).
  • Noonin C , ThongboonkerdV. Exosome–inflammasome crosstalk and their roles in inflammatory responses. Theranostics11(9), 4436–4451 (2021).
  • Tafrihi M , HasheminasabE. miRNAs: biology, biogenesis, their web-based tools, and databases. Microrna8(1), 4–27 (2019).
  • Zuo Y , ChenL, HeXet al. Atorvastatin regulates MALAT1/miR-200c/NRF2 activity to protect against podocyte pyroptosis induced by high glucose. Diabetes Metab. Syndr. Obes.14, 1631–1645 (2021).
  • He F , PengF, XiaXet al. miR-135a promotes renal fibrosis in diabetic nephropathy by regulating TRPC1. Diabetologia57(8), 1726–1736 (2014).
  • Chen YQ , WangXX, YaoXMet al. MicroRNA-195 promotes apoptosis in mouse podocytes via enhanced caspase activity driven by BCL2 insufficiency. Am. J. Nephrol.34(6), 549–559 (2011).
  • Lu Y , LiuD, FengQ, LiuZ. Diabetic nephropathy: perspective on extracellular vesicles. Front. Immunol.11, 943 (2020).
  • Mohan A , SinghRS, KumariMet al. Urinary exosomal microRNA-451-5p is a potential early biomarker of diabetic nephropathy in rats. PLOS ONE11(4), e0154055 (2016).
  • Kim H , BaeYU, JeonJSet al. The circulating exosomal microRNAs related to albuminuria in patients with diabetic nephropathy. J. Transl. Med.17(1), 236 (2019).
  • Xie Y , JiaY, XieCet al. Corrigendum to ‘Urinary exosomal microRNA profiling in incipient type 2 diabetic kidney disease’. J. Diabetes Res.2018, 5969714 (2018).
  • Prabu P , RomeS, SathishkumarCet al. MicroRNAs from urinary extracellular vesicles are non-invasive early biomarkers of diabetic nephropathy in type 2 diabetes patients with the ‘Asian Indian phenotype’. Diabetes Metab.45(3), 276–285 (2019).
  • Wang H , WangJ, LiuT, LengY, YangW. Stem cell-derived exosomal microRNAs: potential therapies in diabetic kidney disease. Biomed. Pharmacother.164, 114961 (2023).
  • Jin J , WangY, ZhaoLet al. Exosomal miRNA-215-5p derived from adipose-derived stem cells attenuates epithelial–mesenchymal transition of podocytes by inhibiting ZEB2. Biomed. Res. Int.2020, 2685305 (2020).
  • Hao Y , MiaoJ, LiuWet al. Mesenchymal stem cell-derived exosomes carry microRNA-125a to protect against diabetic nephropathy by targeting histone deacetylase 1 and downregulating endothelin-1. Diabetes Metab. Syndr. Obes.14, 1405–1418 (2021).
  • Duan Y , ChenB, ChenFet al. Exosomal microRNA-16-5p from human urine-derived stem cells ameliorates diabetic nephropathy through protection of podocyte. J. Cell. Mol. Med.25(23), 10798–10813 (2019).
  • Cai X , ZouF, XuanR, LaiX. Exosomes from mesenchymal stem cells expressing microribonucleic acid-125b inhibit the progression of diabetic nephropathy via the tumour necrosis factor receptor-associated factor 6/Akt axis. Endocr. J.68(7), 817–828 (2021).
  • Akers JC , GondaD, KimR, CarterBS, ChenCC. Biogenesis of extracellular vesicles (EV): exosomes, microvesicles, retrovirus-like vesicles, and apoptotic bodies. J. Neurooncol.113(1), 1–11 (2013).
  • Zhang L , YuD. Exosomes in cancer development, metastasis, and immunity. Biochim. Biophys. Acta Rev. Cancer1871(2), 455–468 (2019).
  • Lin J , LiJ, HuangBet al. Exosomes: novel biomarkers for clinical diagnosis. Sci. World J.2015, 657086 (2015).
  • Zhang H , FreitasD, KimHSet al. Identification of distinct nanoparticles and subsets of extracellular vesicles by asymmetric flow field-flow fractionation. Nat. Cell Biol.20(3), 332–343 (2018).
  • Bowers EC , HassaninAAI, RamosKS. In vitro models of exosome biology and toxicology: new frontiers in biomedical research. Toxicol. In Vitro64, 104462 (2020).
  • Tkach M , ThéryC. Communication by extracellular vesicles: where we are and where we need to go. Cell164(6), 1226–1232 (2016).
  • Li S , WuY, DingFet al. Engineering macrophage-derived exosomes for targeted chemotherapy of triple-negative breast cancer. Nanoscale12(19), 10854–10862 (2020).
  • Duan L , XuL, XuXet al. Exosome-mediated delivery of gene vectors for gene therapy. Nanoscale13(3), 1387–1397 (2021).
  • Meldolesi J . Exosomes and ectosomes in intercellular communication. Curr. Biol.28(8), R435–R444 (2018).
  • Merchant ML , RoodIM, DeegensJKJ, KleinJB. Isolation and characterization of urinary extracellular vesicles: implications for biomarker discovery. Nat. Rev. Nephrol.13(12), 731–749 (2017).
  • Lakhter AJ , PrattRE, MooreREet al. Beta cell extracellular vesicle miR-21-5p cargo is increased in response to inflammatory cytokines and serves as a biomarker of type 1 diabetes. Diabetologia61(5), 1124–1134 (2018).
  • Chang W , WangJ. Exosomes and their noncoding RNA cargo are emerging as new modulators for diabetes mellitus. Cells8(8), 853 (2019).
  • Gauthier BR , Cobo-VuilleumierN, López-NoriegaL. Roles of extracellular vesicles associated non-coding RNAs in diabetes mellitus. Front. Endocrinol.13, 1057407 (2022).
  • Chaput N , ThéryC. Exosomes: immune properties and potential clinical implementations. Semin. Immunopathol.33(5), 419–440 (2011).
  • Cortez MA , Bueso-RamosC, FerdinJet al. MicroRNAs in body fluids – the mix of hormones and biomarkers. Nat. Rev. Clin. Oncol.8(8), 467–477 (2011).
  • Valadi H , EkströmK, BossiosAet al. Exosome-mediated transfer of mRNAs and microRNAs is a novel mechanism of genetic exchange between cells. Nat. Cell Biol.9(6), 654–659 (2007).
  • Guay C , RegazziR. Circulating microRNAs as novel biomarkers for diabetes mellitus. Nat. Rev. Endocrinol.9(9), 513–521 (2013).
  • Karolina DS , TavintharanS, ArmugamAet al. Circulating miRNA profiles in patients with metabolic syndrome. J. Clin. Endocrinol. Metab.97(12), E2271–E2276 (2012).
  • Eissa S , MatboliM, BekhetMM. Clinical verification of a novel urinary microRNA panal: 133b, -342 and -30 as biomarkers for diabetic nephropathy identified by bioinformatics analysis. Biomed. Pharmacother.83, 92–99 (2016).
  • Jia Y , GuanM, ZhengZet al. miRNAs in urine extracellular vesicles as predictors of early-stage diabetic nephropathy. J. Diabetes Res.2016, 7932765 (2016).
  • Park S , LeeK, ParkIBet al. The profiles of microRNAs from urinary extracellular vesicles (EVs) prepared by various isolation methods and their correlation with serum EV microRNAs. Diabetes Res. Clin. Pract.160, 108010 (2020).
  • Zhang W , ZhouX, ZhangHet al. Extracellular vesicles in diagnosis and therapy of kidney diseases. Am. J. Physiol. Renal Physiol.311(5), F844–F851 (2016).
  • Delić D , EiseleC, SchmidRet al. Urinary exosomal miRNA signature in type II diabetic nephropathy patients. PLOS ONE11(3), e0150154 (2016).
  • Florijn BW , DuijsJ, LevelsJHet al. Diabetic nephropathy alters the distribution of circulating angiogenic microRNAs among extracellular vesicles, HDL, and Ago-2. Diabetes68(12), 2287–2300 (2019).
  • Uil M , HauCM, AhdiMet al. Cellular origin and microRNA profiles of circulating extracellular vesicles in different stages of diabetic nephropathy. Clin. Kidney J.14(1), 358–365 (2021).
  • Su H , QiaoJ, HuJet al. Podocyte-derived extracellular vesicles mediate renal proximal tubule cells dedifferentiation via microRNA-221 in diabetic nephropathy. Mol. Cell. Endocrinol.518, 111034 (2020).
  • Jin J , ShiY, GongJet al. Exosome secreted from adipose-derived stem cells attenuates diabetic nephropathy by promoting autophagy flux and inhibiting apoptosis in podocyte. Stem Cell Res. Ther.10(1), 95 (2019).
  • Rayego-Mateos S , Morgado-PascualJL, Opazo-RíosLet al. Pathogenic pathways and therapeutic approaches targeting inflammation in diabetic nephropathy. Int. J. Mol. Sci.21(11), 3798 (2020).
  • Ding X , JingN, ShenAet al. miR-21-5p in macrophage-derived extracellular vesicles affects podocyte pyroptosis in diabetic nephropathy by regulating A20. J. Endocrinol. Invest.44(6), 1175–1184 (2021).
  • Lee SE , JangJE, KimHSet al. Mesenchymal stem cells prevent the progression of diabetic nephropathy by improving mitochondrial function in tubular epithelial cells. Exp. Mol. Med.51(7), 1–14 (2019).
  • Duan Y , LuoQ, WangYet al. Adipose mesenchymal stem cell-derived extracellular vesicles containing microRNA-26a-5p target TLR4 and protect against diabetic nephropathy. J. Biol. Chem.295(37), 12868–12884 (2020).
  • Lv J , HaoYN, WangXP, LuWH, XieLY, NiuD. Bone marrow mesenchymal stem cell-derived exosomal miR-30e-5p ameliorates high-glucose induced renal proximal tubular cell pyroptosis by inhibiting ELAVL1. Ren. Fail.45(1), 2177082 (2023).
  • Gao C , WangB, ChenQet al. Serum exosomes from diabetic kidney disease patients promote pyroptosis and oxidative stress through the miR-4449/HIC1 pathway. Nutr. Diabetes11(1), 33 (2021).
  • Huang Y , LiR, ZhangLet al. Extracellular vesicles from high glucose-treated podocytes induce apoptosis of proximal tubular epithelial cells. Front. Physiol.11, 579296 (2020).
  • Zhang S , WuJ, ZhuXet al. A novel approach to identify the mechanism of miR-145-5p toxicity to podocytes based on the essential genes targeting analysis. Mol. Ther. Nucl. Acids26, 749–759 (2021).
  • Tsai Y , KuoM, HungWet al. High glucose induces mesangial cell apoptosis through miR-15b-5p and promotes diabetic nephropathy by extracellular vesicle delivery. Mol. Ther.28(3), 963–974 (2020).
  • Jiang ZZ , LiuYM, NiuXet al. Exosomes secreted by human urine-derived stem cells could prevent kidney complications from type I diabetes in rats. Stem Cell. Res. Ther.7, 24 (2016).
  • Nagaishi K , MizueY, ChikenjiTet al. Mesenchymal stem cell therapy ameliorates diabetic nephropathy via the paracrine effect of renal trophic factors including exosomes. Sci. Rep.6, 34842 (2016).
  • Liu T , JinQ, YangLet al. Regulation of autophagy by natural polyphenols in the treatment of diabetic kidney disease: therapeutic potential and mechanism. Front. Endocrinol.14, 1142276 (2023).
  • Shapouri-Moghaddam A , MohammadianS, VaziniHet al. Macrophage plasticity, polarization, and function in health and disease. J. Cell. Physiol.233(9), 6425–6440 (2018).
  • Huang H , LiuH, TangJet al. M2 macrophage-derived exosomal miR-25-3p improves high glucose-induced podocytes injury through activation autophagy via inhibiting DUSP1 expression. IUBMB Life72(12), 2651–2662 (2020).
  • Hu R , LiX, PengCet al. miR-196b-5p-enriched extracellular vesicles from tubular epithelial cells mediated aldosterone-induced renal fibrosis in mice with diabetes. BMJ Open Diabetes Res. Care8(1), e001101 (2020).
  • Jin J , QianF, ZhengDet al. Mesenchymal stem cells attenuate renal fibrosis via exosomes-mediated delivery of microRNA let-7i-5p antagomir. Int. J. Nanomed.16, 3565–3578 (2021).
  • Liu D , LiuF, LiZet al. HNRNPA1-mediated exosomal sorting of miR-483-5p out of renal tubular epithelial cells promotes the progression of diabetic nephropathy-induced renal interstitial fibrosis. Cell Death Dis.12(3), 255 (2021).
  • Zhong L , LiaoG, WangXet al. Mesenchymal stem cells-microvesicle-miR-451a ameliorate early diabetic kidney injury by negative regulation of P15 and P19. Exp. Biol. Med.243(15–16), 1233–1242 (2018).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.