Intercellular Communication in Atherosclerosis

Abstract

Cell-to-cell communication is a process necessary for physiological tissue homeostasis and appears often altered during disease. Gap junction channels, formed by connexins, allow the direct intercellular communication between adjacent cells. After a brief review of the pathophysiology of atherosclerosis, we will discuss the role of connexins throughout the different stages of the disease.

Microparticles

“…8,41 Principally, 2 main mechanisms by which MPs mediate 45 Based on their ability to transfer part of their components and content to target cells, MPs quantitatively and qualitatively complement traditional methods of intercellular communication such as direct secretion of signaling molecules, physical interaction of membrane proteins and involvement of gap junctions. 46 This MP-based transcellular delivery system establishes an integrated communication network in which specific properties and information among cells can be rapidly shared and complex processes such as immunoregulation and maintenance of vascular hemostatic balance can be more efficiently coordinated. Notably, under certain pathophysiological conditions, MPs may thus also perpetuate and aggravate deleterious local and general processes such as inflammation, thrombosis, and metastatic spread of cancer.…”

Macro-scale phenomena of arterial coupled cells: a massively parallel simulation

“…SMCs, however, remain homocellularly coupled via all three media. This simulates intercellular coupling in an advanced atheroma especially at the shoulder of the atheroma where expressions of Cx37 and Cx40 are severely downregulated and Cx43 is upregulated in ECs [31,32]. Thus, we see the propagation of a Ca 2þ wave from SMCs provided with a relatively higher amount of agonist flux to those at positions where overlying ECs experience low agonist concentration.…”

“…3 coupling, in addition to the default EC homocellular coupling, is implemented to simulate upregulation of Cx43 in lesion-prone areas [32,33]. Table 3 lists the modes of coupling considered in the four cases taken into account in this study.…”

Plaque, Platelets, and Plug – The Pathogenesis of Acute Coronary Syndrome

“…This native LDL does not initiate an inflammatory response and is not phagocytosed by monocytes, thus does not induce atherosclerosis (Torzewsky & Lackner, 2006). As the plaque progress, fibrous cap is thinner and turn out to be fragile due to the imbalance of extracellular matrix metabolism, the infiltration of the fibrous cap by macrophages and foam cells, and the calcification process (Burnier et al, 2009). All of these contribute to fibrous cap weakening and lost its protective role.…”