关键词: endothelial dysfunction endothelial-to-mesenchymal cell transition fibrocytes hepatic stellate cells myofibroblasts pathological scars pericytes soft tissue fibrosis vascular involvement

Mesh : Animals Cell Communication Cicatrix / pathology Connective Tissue / blood supply pathology Endothelial Cells / metabolism Endothelium / metabolism pathology Fibroblasts / metabolism pathology Fibrosis Hepatic Stellate Cells / cytology metabolism Humans Myofibroblasts / metabolism pathology Neovascularization, Pathologic Organ Specificity Pericytes / metabolism

来  源:   DOI:10.3390/ijms21072542   PDF(Sci-hub)   PDF(Pubmed)

Abstract:
Soft tissue fibrosis in important organs such as the heart, liver, lung, and kidney is a serious pathological process that is characterized by excessive connective tissue deposition. It is the result of chronic but progressive accumulation of fibroblasts and their production of extracellular matrix components such as collagens. Research on pathological scars, namely, hypertrophic scars and keloids, may provide important clues about the mechanisms that drive soft tissue fibrosis, in particular the vascular involvement. This is because these dermal fibrotic lesions bear all of the fibrotic characteristics seen in soft tissue fibrosis. Moreover, their location on the skin surface means they are readily observable and directly treatable and therefore more accessible to research. We will focus here on the roles that blood vessel-associated cells play in cutaneous scar pathology and assess from the literature whether these cells also contribute to other soft tissue fibroses. These cells include endothelial cells, which not only exhibit aberrant functions but also differentiate into mesenchymal cells in pathological scars. They also include pericytes, hepatic stellate cells, fibrocytes, and myofibroblasts. This article will review with broad strokes the roles that these cells play in the pathophysiology of different soft tissue fibroses. We hope that this brief but wide-ranging overview of the vascular involvement in fibrosis pathophysiology will aid research into the mechanisms underlying fibrosis and that this will eventually lead to the development of interventions that can prevent, reduce, or even reverse fibrosis formation and/or progression.
摘要:
重要器官如心脏的软组织纤维化,肝脏,肺,肾脏是一个严重的病理过程,其特征是过度的结缔组织沉积。它是成纤维细胞慢性但进行性积累及其产生细胞外基质组分如胶原的结果。病理性疤痕的研究,即,肥厚性疤痕和瘢痕疙瘩,可能提供有关导致软组织纤维化的机制的重要线索,特别是血管受累。这是因为这些真皮纤维化病变具有在软组织纤维化中看到的所有纤维化特征。此外,它们在皮肤表面的位置意味着它们很容易观察和直接治疗,因此更容易进行研究。我们将在这里集中讨论血管相关细胞在皮肤瘢痕病理中的作用,并从文献中评估这些细胞是否也有助于其他软组织纤维化。这些细胞包括内皮细胞,它不仅表现出异常功能,而且在病理性瘢痕中分化为间充质细胞。它们还包括周细胞,肝星状细胞,纤维细胞,和肌成纤维细胞。本文将广泛回顾这些细胞在不同软组织纤维化的病理生理学中的作用。我们希望,这个简短但广泛的血管参与纤维化病理生理学的概述将有助于研究潜在的纤维化机制,这将最终导致可以预防的干预措施的发展,reduce,或甚至逆转纤维化形成和/或进展。
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