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基质调控瘢痕形成。

Matrix control of scarring.

机构信息

Department of Pathology, University of Pittsburgh, Pittsburgh, PA 15261, USA.

出版信息

Cell Mol Life Sci. 2011 Jun;68(11):1871-81. doi: 10.1007/s00018-011-0663-0. Epub 2011 Mar 10.

Abstract

Repair of wounds usually results in restoration of organ function, even if suboptimal. However, in a minority of situations, the healing process leads to significant scarring that hampers homeostasis and leaves the tissue compromised. This scar is characterized by an excess of matrix deposition that remains poorly organized and weakened. While we know much of the early stages of the repair process, the transition to wound resolution that limits scar formation is poorly understood. This is particularly true of the inducers of scar formation. Here, we present a hypothesis that it is the matrix itself that is a primary driver of scar, rather than being simply the result of other cellular dysregulations.

摘要

伤口的修复通常会导致器官功能的恢复,即使不是最佳状态。然而,在少数情况下,愈合过程会导致明显的瘢痕形成,从而阻碍内稳态并使组织受损。这种瘢痕的特征是基质沉积过多,组织仍然排列不良且脆弱。虽然我们对修复过程的早期阶段了解很多,但对限制瘢痕形成的伤口愈合的转变知之甚少。这在瘢痕形成的诱导剂方面尤其如此。在这里,我们提出了一个假设,即基质本身是瘢痕的主要驱动因素,而不仅仅是其他细胞失调的结果。

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