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首页> 外文期刊>Current opinion in lipidology >Control of smooth muscle cell proliferation in vascular disease.
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Control of smooth muscle cell proliferation in vascular disease.

机译:控制血管疾病中平滑肌细胞的增殖。

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PURPOSE OF REVIEW: Smooth muscle cell proliferation has previously been regarded as a central feature in vascular disease. The role of this process has recently been substantially re-evaluated, and we have reconsidered the functional importance of smooth muscle cell proliferation, the origin of proliferating smooth muscle cells in lesions, and the mechanisms whereby smooth muscle cell proliferation is controlled. In this review, we summarize recent progress in the understanding of smooth muscle cell proliferation, with a particular focus on how interactions between the extracellular matrix, smooth muscle cells, and mitogens control critical steps in this process. RECENT FINDINGS: Irrespective of the origin of smooth muscle cells in vascular lesions, fundamental interactions between the extracellular matrix and cell surface integrins are necessary in order to initiate a proliferative response in a quiescent smooth muscle cell, in a similar manner to any non-malignant cell. These interactions trigger intracellular signaling and cell cycle entry, which facilitate cell cycle progression and proliferation by mitogens. In addition, extracellular matrix interactions may also control the availability and activity of growth factors such as heparin-binding mitogens, which can be sequestered by heparan sulfate containing extracellular matrix components and regulate smooth muscle cell proliferation. SUMMARY: New insights into mechanisms whereby the extracellular matrix takes part in the control of smooth muscle cell proliferation suggest a number of putative targets for future therapies that can be applied to increase plaque stability, prevent the clinical consequences of atherosclerosis and improve outcomes after interventional procedures and organ transplantation.
机译:审查目的:平滑肌细胞增殖以前被认为是血管疾病的主要特征。最近对该过程的作用进行了实质性的重新评估,我们已经重新考虑了平滑肌细胞增殖的功能重要性,病变中平滑肌细胞增殖的起源以及控制平滑肌细胞增殖的机制。在这篇综述中,我们总结了对平滑肌细胞增殖的理解的最新进展,特别关注了细胞外基质,平滑肌细胞和促细胞分裂剂之间的相互作用如何控制这一过程中的关键步骤。最近的发现:不论血管病变中平滑肌细胞的起源如何,胞外基质与细胞表面整合素之间的基本相互作用都是必要的,以便以与任何非恶性肿瘤相似的方式在静止的平滑肌细胞中引发增殖反应。细胞。这些相互作用触发细胞内信号传导和细胞周期进入,从而促进细胞周期的发展和有丝分裂原的增殖。另外,细胞外基质相互作用还可以控制生长因子如肝素结合的有丝分裂原的可用性和活性,所述生长因子可以被含有细胞外基质成分的硫酸乙酰肝素隔离并调节平滑肌细胞增殖。摘要:对细胞外基质参与控制平滑肌细胞增殖的机制的新见解表明,未来疗法的许多假定目标可用于增加斑块稳定性,预防动脉粥样硬化的临床后果并改善介入治疗后的结局和器官移植。

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