The mechanisms that modulate the response to tissue injury are not fully understood. Abnormalities in the repair response are associated with a variety of chronic disease states characterized by inflammation, followed subsequently by excessive ECM deposition. As cell-matrix interactions are able to regulate cellular homeostasis, modification of ECM integrity appears to be an unspecific factor in promoting the onset and progression of inflammatory diseases. Evidence is emerging to show that endogenous ECM molecules supply signals to damage tissues and cells in order to promote further ECM degradation and inflammation progression. Several investigations have been confirmed that HA fragments of different molecular sizes exhibit different biological effects and responses. In fact, the increased deposition of HA into the ECM is a strong hallmark of inflammation processes. In the context of inflammatory pathologies, highly polymerized HA is broken down into small components, which are able to exacerbate the inflammatory response by inducing the release of various detrimental mediators such as reactive oxygen species, cytokines, chemokines and destructive enzymes and by facilitating the recruitment of leukocytes. However, strategies involving the modulation of the HA fragment with specific receptors on cell surface could represent different promising effects for therapeutic scope. This review will focus on the inflammation action of small HA fragments in recent years obtained by in vivo reports.

中文翻译：

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炎性病理过程中的透明质酸断裂：增强组织损伤的信号。

尚未完全了解调节对组织损伤的反应的机制。修复反应异常与多种慢性疾病相关，其特征在于炎症，随后是过多的ECM沉积。由于细胞-基质相互作用能够调节细胞稳态，因此，ECM完整性的修饰似乎是促进炎症性疾病发作和发展的非特异性因素。越来越多的证据表明内源性ECM分子会向损伤的组织和细胞提供信号，从而促进ECM的进一步降解和炎症进程。多项研究已经证实，不同分子大小的HA片段表现出不同的生物学效应和响应。事实上，HA在ECM中的沉积增加是炎症过程的重要标志。在炎症性疾病的背景下，高度聚合的HA被分解成小的成分，它们能够通过诱导释放各种有害介质（例如活性氧，细胞因子，趋化因子和破坏性酶）并促进募集来加剧炎症反应白细胞。然而，涉及用细胞表面上的特定受体调节HA片段的策略对于治疗范围可能代表不同的有希望的效果。该综述将集中于近年来体内报告中获得的小HA片段的炎症作用。它们能够通过诱导各种有害介质如活性氧，细胞因子，趋化因子和破坏性酶的释放以及促进白细胞募集而加剧炎症反应。然而，涉及用细胞表面上的特定受体调节HA片段的策略对于治疗范围可能代表不同的有希望的效果。该综述将集中于近年来体内报告中获得的小HA片段的炎症作用。它们能够通过诱导各种有害介质如活性氧，细胞因子，趋化因子和破坏性酶的释放以及促进白细胞募集而加剧炎症反应。然而，涉及用细胞表面上的特定受体调节HA片段的策略对于治疗范围可能代表不同的有希望的效果。该综述将集中于近年来体内报告中获得的小HA片段的炎症作用。涉及用细胞表面的特定受体调节HA片段的策略可能代表治疗范围的不同前景。该综述将集中于近年来体内报告中获得的小HA片段的炎症作用。涉及用细胞表面上的特定受体调节HA片段的策略可能代表治疗范围的不同前景。该综述将集中于近年来体内报告中获得的小HA片段的炎症作用。