非编码RNA调控糖尿病创面愈合机制的研究进展

李晓亮; 谢江帆; 叶向阳; 李琰光; 刘德伍

doi:10.3760/cma.j.cn501225-20221101-00477

非编码RNA调控糖尿病创面愈合机制的研究进展

doi: 10.3760/cma.j.cn501225-20221101-00477

1.
郑州市第一人民医院烧伤科，郑州　　450004
2.
南昌大学第一附属医院烧伤整形与创面修复医学中心，南昌　　330006

基金项目:

河南省医学科技攻关项目 LHGJ20200700, LHGJ20210714

详细信息

通讯作者:
刘德伍，Email：dewuliu@126.com

计量
- 文章访问数: 282
- HTML全文浏览量: 56
- PDF下载量: 22
- 被引次数: 0
出版历程
- 收稿日期: 2022-11-01

Research advances on the mechanism of non-coding RNA regulated diabetic wound healing

1.
Department of Burns, Zhengzhou First People's Hospital, Zhengzhou 450004, China
2.
Medical Center of Burn Plastic and Wound Repair, the First Affiliated Hospital of Nanchang University, Nanchang 330006, China

Funds:

Henan Medical Science and Technology Project LHGJ20200700, LHGJ20210714

More Information

Corresponding author: Liu Dewu, Email: dewuliu@126.com

摘要

摘要: 糖尿病创面是糖尿病患者的常见并发症，近年来其发病率不断上升，且临床预后较差，严重影响患者的生活质量，逐渐成为糖尿病治疗的重点和难点。非编码RNA作为调控基因表达的RNA，可调控许多疾病的病理生理过程，在糖尿病创面的愈合过程中起着重要作用。该文对3种常见非编码RNA在糖尿病创面愈合过程中的调控作用、诊断价值、治疗潜力进行了综述，从基因层面和分子水平上为糖尿病创面的诊疗提供了新思路。
- 糖尿病 /
- RNA，长链非编码 /
- 伤口愈合
Abstract: Diabetic wounds are a common complication of diabetic patients, and the incidence has been increasing in recent years. In addition, its poor clinical prognosis seriously affects the quality of life of patients, which has become the focus and difficulty of diabetes treatment. As the RNA regulating gene expression, non-coding RNA can regulate the pathophysiological process of diseases, and play an important role in the healing process of diabetic wounds. In this paper, we reviewed the regulatory role, diagnostic value, and therapeutic potential of three common non-coding RNA in diabetic wounds, in order to provide a new solution for the diagnosis and treatment of diabetic wounds at the genetic and molecular level.
- Diabetes mellitus /
- RNA, long noncoding /
- Wound healing
所有作者均声明不存在利益冲突

HTML全文

参考文献(41)

[1]	XieWG, HuWG, HuangZ, et al. Betulinic acid accelerates diabetic wound healing by modulating hyperglycemia-induced oxidative stress, inflammation and glucose intolerance[J/OL]. Burns Trauma, 2022, 10:tkac007[2022-10-31]. https://pubmed.ncbi.nlm.nih.gov/35415192/. DOI: 10.1093/burnst/tkac007.
[2]	XieWG, ZhouXQ, HuWG, et al. Pterostilbene accelerates wound healing by modulating diabetes-induced estrogen receptor β suppression in hematopoietic stem cells[J/OL]. Burns Trauma, 2021, 9:tkaa045[2022-10-31]. https://pubmed.ncbi.nlm.nih.gov/33654697/. DOI: 10.1093/burnst/tkaa045.
[3]	SinghK, PalD, SinhaM, et al. Epigenetic modification of microRNA-200b contributes to diabetic vasculopathy[J]. Mol Ther, 2017,25(12):2689-2704. DOI: 10.1016/j.ymthe.2017.09.009.
[4]	JinGX, WangQ, HuXL, et al. Profiling and functional analysis of differentially expressed circular RNAs in high glucose-induced human umbilical vein endothelial cells[J]. FEBS Open Bio, 2019,9(9):1640-1651. DOI: 10.1002/2211-5463.12709.
[5]	RenHY, ZhaoF, ZhangQQ, et al. Autophagy and skin wound healing[J/OL]. Burns Trauma, 2022, 10:tkac003[2022-10-31]. https://pubmed.ncbi.nlm.nih.gov/35187180/. DOI: 10.1093/burnst/tkac003.
[6]	LiX,LiN,LiBX,et al.Noncoding RNAs and RNA-binding proteins in diabetic wound healing[J].Bioorg Med Chem Lett,2021,50:128311.DOI: 10.1016/j.bmcl.2021.128311.
[7]	LiSY, YangP, DingXF, et al. Puerarin improves diabetic wound healing via regulation of macrophage M2 polarization phenotype[J/OL]. Burns Trauma, 2022, 10:tkac046[2022-10-31]. https://pubmed.ncbi.nlm.nih.gov/36568527/. DOI: 10.1093/burnst/tkac046.
[8]	WuXQ, HeWJ, MuXR, et al. Macrophage polarization in diabetic wound healing[J/OL]. Burns Trauma, 2022, 10:tkac051[2022-10-31]. https://pubmed.ncbi.nlm.nih.gov/36601058/. DOI: 10.1093/burnst/tkac051.
[9]	HuJY, ZhangLP, LiechtyC, et al. Long noncoding RNA GAS5 regulates macrophage polarization and diabetic wound healing[J]. J Invest Dermatol, 2020,140(8):1629-1638. DOI: 10.1016/j.jid.2019.12.030.
[10]	DingJX,GaoBB,ChenZH,et al.An NIR-triggered Au nanocage used for photo-thermo therapy of chronic wound in diabetic rats through bacterial membrane destruction and skin cell mitochondrial protection[J].Front Pharmacol,2021,12:779944.DOI: 10.3389/fphar.2021.779944.
[11]	ZgheibC, HodgesMM, HuJY, et al. Long non-coding RNA Lethe regulates hyperglycemia-induced reactive oxygen species production in macrophages[J]. PLoS One, 2017,12(5):e0177453. DOI: 10.1371/journal.pone.0177453.
[12]	XuSJ, WengXY, WangY, et al. Screening and preliminary validation of T lymphocyte immunoregulationassociated long noncoding RNAs in diabetic foot ulcers[J]. Mol Med Rep, 2019,19(3):2368-2376. DOI: 10.3892/mmr.2019.9877.
[13]	UmeharaT, MoriR, MaceKA, et al. Identification of specific miRNAs in neutrophils of type 2 diabetic mice: overexpression of miRNA-129-2-3p cccelerates diabetic wound healing[J]. Diabetes, 2019,68(3):617-630. DOI: 10.2337/db18-0313.
[14]	WangJ, WangX, WangLF, et al. MiR-let-7d-3p regulates IL-17 expression through targeting AKT1/mTOR signaling in CD4+ T cells[J]. In Vitro Cell Dev Biol Anim, 2020, 56(1):67-74. DOI: 10.1007/s11626-019-00409-5.
[15]	GeigerA, WalkerA, NissenE. Human fibrocyte-derived exosomes accelerate wound healing in genetically diabetic mice[J]. Biochem Biophys Res Commun, 2015,467(2):303-309. DOI: 10.1016/j.bbrc.2015.09.166.
[16]	BanE,JeongS,ParkM,et al.Accelerated wound healing in diabetic mice by miRNA-497 and its anti-inflammatory activity[J].Biomed Pharmacother,2020,121:109613.DOI: 10.1016/j.biopha.2019.109613.
[17]	ZhangW, SuiY. CircBPTF knockdown ameliorates high glucose-induced inflammatory injuries and oxidative stress by targeting the miR-384/LIN28B axis in human umbilical vein endothelial cells[J]. Mol Cell Biochem, 2020,471(1/2):101-111. DOI: 10.1007/s11010-020-03770-2.
[18]	ChenJJ, CuiLQ, YuanJL, et al. Circular RNA WDR77 target FGF-2 to regulate vascular smooth muscle cells proliferation and migration by sponging miR-124[J]. Biochem Biophys Res Commun, 2017,494(1/2):126-132. DOI: 10.1016/j.bbrc.2017.10.068.
[19]	ZhangX,ChenL,XiaoB,et al.Circ_0075932 in adipocyte-derived exosomes induces inflammation and apoptosis in human dermal keratinocytes by directly binding with PUM2 and promoting PUM2-mediated activation of AuroraA/NF-κB pathway[J].Biochem Biophys Res Commun,2019,511(3):551-558.DOI: 10.1016/j.bbrc.2019.02.082.
[20]	YanCQ, ChenJ, WangC, et al. Milk exosomes-mediated miR-31-5p delivery accelerates diabetic wound healing through promoting angiogenesis[J]. Drug Deliv, 2022,29(1):214-228. DOI: 10.1080/10717544.2021.2023699.
[21]	LiB,ZhouY,ChenJ,et al.Long non-coding RNA H19 contributes to wound healing of diabetic foot ulcer[J].J Mol Endocrinol,2020,65(3): 69-84.DOI: 10.1530/JME-19-0242.
[22]	AlfaifiM, VermaAK, AlshahraniMY, et al. Assessment of cell-free long non-coding RNA-H19 and miRNA-29a, miRNA-29b expression and severity of diabetes[J]. Diabetes Metab Syndr Obes, 2020,13:3727-3737. DOI: 10.2147/DMSO.S273586.
[23]	WangJM, TaoJ, ChenDD, et al. MicroRNA miR-27b rescues bone marrow-derived angiogenic cell function and accelerates wound healing in type 2 diabetes mellitus[J]. Arterioscler Thromb Vasc Biol, 2014,34(1):99-109. DOI: 10.1161/ATVBAHA.113.302104.
[24]	XuXB, ZhangHT, LiJH, et al. Combination of EPC-EXs and NPC-EXs with miR-126 and miR-210 overexpression produces better therapeutic effects on ischemic stroke by protecting neurons through the Nox2/ROS and BDNF/TrkB pathways[J]. Exp Neurol, 2023,359:114235. DOI: 10.1016/j.expneurol.2022.114235.
[25]	AminKN,UmapathyD,AnandharajA,et al.miR-23c regulates wound healing by targeting stromal cell-derived factor-1α (SDF-1α/CXCL12) among patients with diabetic foot ulcer[J].Microvasc Res,2020,127:103924.DOI: 10.1016/j.mvr.2019.103924.
[26]	ZhengJJ,MaoYQ,DongPH,et al.Long noncoding RNA HOTTIP mediates SRF expression through sponging miR-150 in hepatic stellate cells[J].J Cell Mol Med,2019,23(2):1572-1580.DOI: 10.1111/jcmm.14068.
[27]	ZouJ, LiuKC, WangWP, et al. Circular RNA COL1A2 promotes angiogenesis via regulating miR-29b/VEGF axis in diabetic retinopathy[J]. Life Sci, 2020,256:117888. DOI: 10.1016/j.lfs.2020.117888.
[28]	LiuXQ,DuanLS,ChenYQ,et al.lncRNA MALAT1 accelerates wound healing of diabetic mice transfused with modified autologous blood via the HIF-1α signaling pathway[J].Mol Ther Nucleic Acids,2019,17:504-515.DOI: 10.1016/j.omtn.2019.05.020.
[29]	HuMD, WuYX, YangC, et al. Novel long noncoding RNA lnc-URIDS delays diabetic wound healing by targeting Plod1[J]. Diabetes, 2020,69(10):2144-2156. DOI: 10.2337/db20-0147.
[30]	ZhouLY, RenM, ZengTT, et al. TET2-interacting long noncoding RNA promotes active DNA demethylation of the MMP-9 promoter in diabetic wound healing[J]. Cell Death Dis, 2019,10(11):813. DOI: 10.1038/s41419-019-2047-6.
[31]	YuanLQ, SunY, XuML, et al. miR-203 acts as an inhibitor for epithelial-mesenchymal transition process in diabetic foot ulcers via targeting interleukin-8[J]. Neuroimmunomodulation, 2019,26(5):239-249. DOI: 10.1159/000503087.
[32]	MouraJ,SørensenA,LealEC,et al.microRNA-155 inhibition restores fibroblast growth factor 7 expression in diabetic skin and decreases wound inflammation[J].Sci Rep,2019,9(1):5836.DOI: 10.1038/s41598-019-42309-4.
[33]	LiB, LuanS, ChenJ, et al. The MSC-derived exosomal lncRNA H19 promotes wound healing in diabetic foot ulcers by upregulating PTEN via MicroRNA-152-3p[J]. Mol Ther Nucleic Acids, 2020,19:814-826. DOI: 10.1016/j.omtn.2019.11.034.
[34]	ZengTT,WangXY,WangW,et al.Endothelial cell-derived small extracellular vesicles suppress cutaneous wound healing through regulating fibroblasts autophagy[J].Clin Sci (Lond),2019,133(9): CS20190008.DOI: 10.1042/CS20190008.
[35]	LinCJ,LanYM,OuMQ,et al.Expression of miR-217 and HIF-1α/VEGF pathway in patients with diabetic foot ulcer and its effect on angiogenesis of diabetic foot ulcer rats[J].J Endocrinol Invest,2019,42(11):1307-1317.DOI: 10.1007/s40618-019-01053-2.
[36]	DangwalS, StratmannB, BangC, et al. Impairment of wound healing in patients with type 2 diabetes mellitus influences circulating microRNA patterns via inflammatory cytokines[J]. Arterioscler Thromb Vasc Biol, 2015,35(6):1480-1488. DOI: 10.1161/ATVBAHA.114.305048.
[37]	XuYX, PuSD, LiX, et al. Exosomal ncRNAs: novel therapeutic target and biomarker for diabetic complications[J]. Pharmacol Res, 2022,178:106135. DOI: 10.1016/j.phrs.2022.106135.
[38]	CaiHA, HuangL, ZhengLJ, et al. Ginsenoside (Rg-1) promoted the wound closure of diabetic foot ulcer through iNOS elevation via miR-23a/IRF-1 axis[J]. Life Sci, 2019,233:116525. DOI: 10.1016/j.lfs.2019.05.081.
[39]	SawayaAP, JozicI, StoneRC, et al. Mevastatin promotes healing by targeting caveolin-1 to restore EGFR signaling[J]. JCI Insight, 2019,4(23):e129320. DOI: 10.1172/jci.insight.129320.
[40]	XiaoX, XuMQ, YuHL, et al. Mesenchymal stem cell-derived small extracellular vesicles mitigate oxidative stress-induced senescence in endothelial cells via regulation of miR-146a/Src[J]. Signal Transduct Target Ther, 2021,6(1):354. DOI: 10.1038/s41392-021-00765-3.
[41]	KaurP, KotruS, SinghS, et al. Role of miRNAs in diabetic neuropathy: mechanisms and possible interventions[J]. Mol Neurobiol, 2022,59(3):1836-1849. DOI: 10.1007/s12035-021-02662-w.