MicroRNA as Therapeutic Targets for Chronic Wound Healing

被引:96
作者
Mulholland, Eoghan J. [1 ]
Dunne, Nicholas [1 ,2 ,3 ,4 ]
McCarthy, Helen O. [1 ]
机构
[1] Queens Univ Belfast, Sch Pharm, 97 Lisburn Rd, Belfast BT9 7BL, Antrim, North Ireland
[2] Dublin City Univ, Sch Mech & Mfg Engn, Ctr Med Engn Res, Stokes Bldg,Collins Ave, Dublin 9, Ireland
[3] Trinity Coll Dublin, Trinity Biomed Sci Inst, Trinity Ctr Bioengn, Dublin 2, Ireland
[4] Trinity Coll Dublin, Sch Engn, Dept Mech & Mfg Engn, Dublin 2, Ireland
来源
MOLECULAR THERAPY-NUCLEIC ACIDS | 2017年 / 8卷
关键词
PROMOTES KERATINOCYTE MIGRATION; HUMAN ENDOTHELIAL-CELLS; GROWTH-FACTOR; NITRIC-OXIDE; COLLAGEN EXPRESSION; DIABETIC-RATS; LUNG-CANCER; HUMAN SKIN; FACTOR-I; ANGIOGENESIS;
D O I
10.1016/j.omtn.2017.06.003
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Wound healing is a highly complex biological process composed of three overlapping phases: inflammation, proliferation, and remodeling. Impairments at any one or more of these stages can lead to compromised healing. MicroRNAs (miRs) are non-coding RNAs that act as post-transcriptional regulators of multiple proteins and associated pathways. Thus, identification of the appropriate miR involved in the different phases of wound healing could reveal an effective third-generation genetic therapy in chronic wound care. Several miRs have been shown to be upregulated or downregulated during the wound healing process. This article examines the biological processes involved in wound healing, the miR involved at each stage, and how expression levels are modulated in the chronic wound environment. Key miRs are highlighted as possible therapeutic targets, either through underexpression or overexpression, and the healing benefits are interrogated. These are prime miR candidates that could be considered as a gene therapy option for patients suffering from chronic wounds. The success of miR as a gene therapy, however, is reliant on the development of an appropriate delivery system that must be designed to overcome both extracellular and intracellular barriers.
引用
收藏
页码:46 / 55
页数:10
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