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程序性细胞死亡的分子影像学研究进展:第一部分——病理生理学和放射性示踪剂。

Recent advances in the molecular imaging of programmed cell death: part I--pathophysiology and radiotracers.

机构信息

Division of Pediatric Radiology, Department of Radiology, Lucile Salter Packard Children's Hospital, Stanford, CA, USA.

出版信息

J Nucl Med. 2012 Nov;53(11):1659-62. doi: 10.2967/jnumed.112.108944. Epub 2012 Oct 2.

DOI:10.2967/jnumed.112.108944
PMID:23033360
Abstract

In humans, apoptosis (programmed cell death) is the most common form of cell death after necrosis. Apoptosis is a series of genetically preprogrammed biochemical and morphologic energy-requiring events that, after a specific external or internal stimulus, results in the physiologic disappearance of a cell via its self-disintegration and packaging of its contents into membrane vesicles called apoptotic bodies. Apoptotic bodies can readily be ingested, with their nutrients and even organelles recycled by neighboring cells or phagocytes without local inflammation. In contrast, necrosis is characterized by the primary loss of plasma membrane integrity and the uncontrolled release of a cell's contents, often causing local inflammation, tissue damage, and scarring. Alternate forms of cell death also exist, associated with specific molecular mechanisms involving enzymes, organelles, genes, external stimuli, or blockade of normal cell proliferation. In this review we will briefly outline the molecular mechanisms of apoptosis that can be imaged with radiotracers now under development.

摘要

在人类中,细胞凋亡(程序性细胞死亡)是坏死后最常见的细胞死亡形式。细胞凋亡是一系列遗传上预先编程的生化和形态学能量需求事件,在特定的外部或内部刺激后,通过细胞自身的解体和将其内容物包装到称为凋亡小体的膜泡中,导致细胞生理性消失。凋亡小体可以被邻近细胞或吞噬细胞轻易地摄取,其营养物质甚至细胞器被回收,而不会引起局部炎症。相比之下,坏死的特征是质膜完整性的主要丧失和细胞内容物的失控释放,通常会导致局部炎症、组织损伤和瘢痕形成。还存在其他形式的细胞死亡,与涉及酶、细胞器、基因、外部刺激或阻断正常细胞增殖的特定分子机制有关。在这篇综述中,我们将简要概述目前正在开发的放射性示踪剂可成像的细胞凋亡的分子机制。

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Recent advances in the molecular imaging of programmed cell death: part I--pathophysiology and radiotracers.程序性细胞死亡的分子影像学研究进展:第一部分——病理生理学和放射性示踪剂。
J Nucl Med. 2012 Nov;53(11):1659-62. doi: 10.2967/jnumed.112.108944. Epub 2012 Oct 2.
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