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首页> 外文期刊>Wound repair and regeneration: official publication of the Wound Healing Society [and] the European Tissue Repair Society >The link between hypertension and pathological scarring: Does hypertension cause or promote keloid and hypertrophic scar pathogenesis?
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The link between hypertension and pathological scarring: Does hypertension cause or promote keloid and hypertrophic scar pathogenesis?

机译:高血压与病理瘢痕形成之间的联系:高血压会导致或促进瘢痕loid和肥厚性瘢痕发病机理吗?

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摘要

Pathological scars, namely, keloids and hypertrophic scars (HSs), are caused by excessive cutaneous wound healing that is characterized by histological extracellular matrix (ECM) accumulation, clinically relevant irritating symptoms, and frequent recurrence after surgical excision. To date, there are few effective and specific treatments. This partly reflects the poor understanding of the etiology of these scars and the lack of a suitable animal model. Systemic hypertension has been suggested to participate in pathological scarring. The evidence that supports this hypothesis is reviewed here. Thus, hypertension associates with changes that resemble the aberrant cutaneous wound-healing phases that characterize pathological scar development. It also associates with profibrotic functional changes in the cells that constitute keloids and HSs (endothelial cells, pericytes/myofibroblasts, dermal fibroblasts, and mast cells) and profibrotic ECM remodeling. These hypertension-associated changes are mediated to some extent by inflammation, hypoxia, and the angiotensin/renin-angiotensin-aldosterone system. Thus, hypertension may be an aggravating/risk factor for keloids and HSs. This will help to identify patients who are prone to heavy scars after surgery or postsurgical recurrence. Moreover, pharmacological agents for the prophylaxis and treatment of hypertension-induced fibrosis in other organs may also be useful for keloids/HSs.
机译:病理性瘢痕,即瘢痕loid和肥厚性瘢痕(HSs),是由皮肤伤口过度愈合引起的,其特征在于组织学细胞外基质(ECM)积累,临床相关的刺激性症状以及手术切除后的频繁复发。迄今为止,几乎没有有效且具体的治疗方法。这部分反映了对这些疤痕病因的了解不足,以及缺乏合适的动物模型。已建议全身性高血压参与病理瘢痕形成。支持该假设的证据在这里进行了综述。因此,高血压伴随着类似于病理性瘢痕发展的异常皮肤伤口愈合阶段的变化。它还与构成瘢痕loid和HS的细胞(内皮细胞,周细胞/肌成纤维细胞,真皮成纤维细胞和肥大细胞)的纤维化功能改变和纤维化ECM重塑相关。这些与高血压相关的变化在一定程度上由炎症,缺氧和血管紧张素/肾素-血管紧张素-醛固酮系统介导。因此,高血压可能是瘢痕loid和HS的加重/危险因素。这将有助于确定在手术后或术后复发后容易出现严重疤痕的患者。此外,用于预防和治疗其他器官中高血压引起的纤维化的药理剂也可用于瘢痕loid / HS。

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