论文标题
内侧损伤/功能障碍诱导的肉芽组织修复是动脉粥样硬化的发病机理
Medial Injury/Dysfunction Induced Granulation Tissue Repair is the Pathogenesis of Atherosclerosis
论文作者
论文摘要
动脉粥样硬化是血管壁的慢性病变，仍然是死亡和生命年丧失的主要原因。长期以来，主要是解释动脉粥样硬化的经典假设。不幸的是，这些假设可能无法解释动脉粥样硬化易感性的差异。在过去的150年中，这些问题引起了争议。检查了人类冠状动脉的动脉粥样硬化，发现培养基的三角形是培养基中细胞损伤的真实肖像画，Intima的三角形是肌纤维细胞增殖，外细胞外基质（ECM）分泌的真实肖像，胶原纤维形成和胶原纤维形成和维修媒介。肌纤维细胞，ECM和管腔（Intima）/Vasa vasorum（VV）（Adventitia）构成肉芽组织修复。随着肉芽组织增生，许多胶原蛋白纤维（正常或变性），泡沫细胞和新的毛细血管形成。因此，假定了以下理论：危险因素诱导平滑肌细胞（SMC）损伤/损失，纤维化或结构破坏可能会在培养基中发展，从而导致培养基功能障碍。培养基功能障碍会促使血管的机械特性受到干扰，从而导致内膜和Addingitia的压力更大。内膜/外膜中的肉芽组织发展以修复受伤的培养基。动脉粥样硬化，僵硬或动脉瘤根据培养基功能障碍的严重程度和肉芽组织修复模式/程度而发展。临床动脉粥样硬化的几乎所有特征都可以用该理论来解释。我们认为，培养基功能障碍是动脉粥样硬化发病机理中的关键引发剂。预计动脉粥样硬化的培养基功能障碍理论应该更好地了解动脉粥样硬化的病因。
Atherosclerosis, a chronic lesion of vascular wall, remains a leading cause of death and loss of life years. Classical hypotheses for atherosclerosis are long-standing mainly to explain atherogenesis. Unfortunately, these hypotheses may not explain the variation in the susceptibility to atherosclerosis. These issues are controversial over the past 150 years. Atherosclerosis from human coronary arteries was examined and triangle of media was found to be a true portraiture of cells injury in the media, and triangle of intima was a true portraiture of myofibroblast proliferation, extracellular matrix (ECM) secretion, collagen fiber formation and intimal thickening to repair media dysfunction. Myofibroblasts, ECM and lumen (intima)/vasa vasorum (VV) (adventitia) constitute granulation tissue repair. With granulation tissue hyperplasia, lots of collagen fibers (normal or denatured), foam cells and new capillaries formed. Thus, the following theory was postulated: Risk factors induce smooth muscle cells (SMCs) injury/loss, and fibrosis or structure destruction could be developed in the media, which lead to media dysfunction. Media dysfunction prompts disturbed mechanical properties of blood vessels, resulting in bigger pressure buildup in the intima and adventitia. Granulation tissues in the intima/adventitia develop to repair the injured media. Atherosclerosis, stiffening or aneurysm develops depending on media dysfunction severity and granulated tissue repair mode/degree. Nearly all characteristics of clinical atherosclerosis could be ideally interpreted with the theory. We believe that media dysfunction is a key initiator in the pathogenesis of atherosclerosis. It is expected that media dysfunction theory of atherosclerosis, should offer better understanding of the etiology for atherosclerosis.
