Perspective Of Inflammation Research Articles

Inflammation and Acute Venous Thrombosis

Inflammation is known as a controlled response to an injury that protects against further injury and clears damaged tissue. However, uncontrolled inflammation can lead to a marked breakdown of the extracellular matrix as well as organ destruction. Stewart et al. demonstrated in a vein thrombosis model that leukocytes migrate into vein walls with an intact layer of endothelial cells, subsequently linking inflammation and thrombosis. Since then, multiple studies have reported on the interaction between inflammation and vein thrombosis. This article summarizes published material that assesses the relationship between inflammation and acute vein thrombosis. The article will focus on the role of endothelial cells, leukocytes, platelets, and microparticles in acute vein thrombosis and discuss the role of thrombin, P-selectin, platelet-activating factor, endothelin-1, and nitric oxide from the perspective of inflammation.

Vascular Angiotensin-Converting Enzyme 2

See related article, pages 888–897 Through the actions of its main biological peptide, angiotensin (Ang) II, the renin–angiotensin system (RAS) has been implicated in atherosclerosis.1,2 The proatherogenic effect of Ang II may involve a variety of proinflammatory mechanisms that are largely independent from its effect on blood pressure.1 Ang II promotes monocyte and endothelial cell activation, as well as leukocyte recruitment and adhesion to the atherosclerotic plaque.3 This peptide also increases vascular oxidative stress, an effect that may also contribute to atherogenesis.4 The formation of Ang II by angiotensin-converting enzyme (ACE)-dependent and ACE-independent pathways has been viewed as the main determinant of systemic and local Ang II levels. With the discovery of ACE2, an enzyme that degrades Ang II, there has been increased interest in the regulation of Ang II levels through the degradation pathway.5,6 ACE2 is a homolog of ACE that cleaves the octapeptide Ang II into Ang-(1-7) by removing a single amino acid phenylalanine from its C-terminal end.7,8 Because of its ability to degrade Ang II, ACE2 is viewed as a counter-regulator of Ang II overactivity.8,9 This property could have therapeutic implications. We suggested that ACE2 could be renoprotective, especially when associated with low levels of ACE.10 Increasing evidence suggests that ACE2 plays a protective role in cardiovascular disease and other pathologies.5,11 In this issue of Circulation Research , Thomas et al12 report their findings of a cross between atherosclerosis-prone apolipoprotein (Apo)E knockout (KO) and ACE2 KO mice to study the effects of ACE2 deficiency on the development of atherosclerosis. Genetic ACE 2 ablation led to enhanced vascular inflammation and plaque formation in ApoE KO mice. In ApoE-replete mice, ACE2 deficiency was also associated with increased expression of …

Perspectives in Inflammation: Future Trends and Developments

Perspectives in Inflammation: Future Trends and Developments

Book Review: Perspectives in Inflammation: Future Trends and Developments

Book Review: Perspectives in Inflammation: Future Trends and Developments

Perspectives in Inflammation.

Perspectives in Inflammation.

Perspectives in Inflammation. Future Trends and Developments

Perspectives in Inflammation. Future Trends and Developments