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Myocardial infarction remodeling that progresses to heart failure: a signaling misunderstanding

机译:心肌梗死的重塑导致心力衰竭:信号传态误解

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摘要

After myocardial infarction, remodeling of the left ventricle involves a wound-healing orchestra involving a variety of cell types. In order for wound healing to be optimal, appropriate communication must occur; these cells all need to come in at the right time, be activated at the right time in the right amount, and know when to exit at the right time. When this occurs, a new homeostasis is obtained within the infarct, such that infarct scar size and quality are sufficient to maintain left ventricular size and shape. The ideal scenario does not always occur in reality. Often, miscommunication can occur between infarct and remote spaces, across the temporal wound-healing spectrum, and across organs. When miscommunication occurs, adverse remodeling can progress to heart failure. This review discusses current knowledge gaps and recent development of the roles of inflammation and the extracellular matrix in myocardial infarction remodeling. In particular, the macrophage is one cell type that provides direct and indirect regulation of both the inflammatory and scar-forming responses. We summarize current research efforts focused on identifying biomarker indicators that reflect the status of each component of the wound-healing process to better predict outcomes.
机译:在心肌梗死后,重塑左心室涉及涉及各种细胞类型的伤口愈合管弦乐队。为了使伤口愈合是最佳的,必须发生适当的沟通;这些细胞都需要在合适的时间进入,在合适的时间在合适的时间激活,并且知道何时在正确的时间退出。发生这种情况时,在梗死中获得新的稳态,使得梗塞瘢痕尺寸和质量足以保持左心室大小和形状。理想的情景并不总是发生在现实中。通常,梗塞和遥控空间之间的误解可能会发生在颞伤的愈合光谱和跨越器官之间。发生误解时,不利的重塑可以进展到心力衰竭。本综述讨论了当前知识差距和最近的炎症作用和细胞外基质在心肌梗死重塑中的作用。特别地,巨噬细胞是一种细胞类型,可提供炎症和瘢痕形成反应的直接和间接调节。我们总结了当前的研究努力,专注于识别反映伤口愈合过程的每个部件状况的生物标志物指标,以更好地预测结果。

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