Pakyari Mohammadreza, Farrokhi Ali, Maharlooei Mohsen Khosravi, Ghahary Aziz
Department of Surgery, University of British Columbia , Vancouver, Canada .
Department of Surgery, University of British Columbia , Vancouver, Canada . ; Professional Fire Fighters' Burn & Wound Healing Research Laboratory, University of British Columbia , Vancouver, Canada .
Adv Wound Care (New Rochelle). 2013 Jun;2(5):215-224. doi: 10.1089/wound.2012.0406.
This review highlights the critical role of transforming growth factor beta (TGF-β)1-3 within different phases of wound healing, in particular, late-stage wound healing. It is also very important to identify the TGF-β1-controlling factors involved in slowing down the healing process upon wound epithelialization.
TGF-β1, as a growth factor, is a known proponent of dermal fibrosis. Several strategies to modulate or regulate TGF's actions have been thoroughly investigated in an effort to create successful therapies. This study reviews current discourse regarding the many roles of TGF-β1 in wound healing by modulating infiltrated immune cells and the extracellular matrix.
It is well established that TGF-β1 functions as a wound-healing promoting factor, and thereby if in excess it may lead to overhealing outcomes, such as hypertrophic scarring and keloid. Thus, the regulation of TGF-β1 in the later stages of the healing process remains as critical issue of which to better understand.
One hypothesis is that cell communication is the key to regulate later stages of wound healing. To elucidate the role of keratinocyte/fibroblast cross talk in controlling the later stages of wound healing we need to: (1) identify those keratinocyte-released factors which would function as wound-healing stop signals, (2) evaluate the functionality of these factors in controlling the outcome of the healing process, and (3) formulate topical vehicles for these antifibrogenic factors to improve or even prevent the development of hypertrophic scarring and keloids as a result of deep trauma, burn injuries, and any type of surgical incision.
本综述强调了转化生长因子β（TGF-β）1-3在伤口愈合不同阶段，尤其是伤口愈合后期的关键作用。识别在伤口上皮化后减缓愈合过程中涉及的TGF-β1调控因子也非常重要。
TGF-β1作为一种生长因子，是已知的真皮纤维化支持者。为了开发成功的治疗方法，已经对几种调节或调控TGF作用的策略进行了深入研究。本研究通过调节浸润的免疫细胞和细胞外基质，综述了目前关于TGF-β1在伤口愈合中多种作用的论述。
TGF-β1作为一种促进伤口愈合的因子已得到充分证实，因此如果过量，它可能导致过度愈合的结果，如肥厚性瘢痕和瘢痕疙瘩。因此，在愈合过程后期对TGF-β1的调控仍然是一个需要更好理解的关键问题。
一种假设是细胞通讯是调节伤口愈合后期的关键。为了阐明角质形成细胞/成纤维细胞相互作用在控制伤口愈合后期的作用，我们需要：（1）识别那些可作为伤口愈合停止信号的角质形成细胞释放因子；（2）评估这些因子在控制愈合过程结果中的功能；（3）为这些抗纤维化因子配制局部载体，以改善甚至预防因深度创伤、烧伤和任何类型的手术切口导致的肥厚性瘢痕和瘢痕疙瘩的形成。
