Related Experiment Video

Updated: Aug 15, 2026

Mouse Models for Graft Arteriosclerosis
07:37

Mouse Models for Graft Arteriosclerosis

Published on: May 14, 2013

[Humoral effectors and cellular targets of chronic arterial wall allorejection]

J B Michel1, D Plissonnier, D Gomes

  • 1Unité 460 de 1'INSERM, CHU X. Bichat, 16 rue Henri Huchard-75018 Paris.

Bulletin De L'Academie Nationale De Medecine
|August 15, 2001
PubMed

Contrasting with acute rejection, chronic rejection of arterial allograft don't involve leukocyte passengers from the graft to the host. Chronic rejection involves the proteins of the major histocompatibility complexes. Experimental studies in rats showed that the process evolved in three stages: a first stage of histo-incompatibility recognition mediated by the graft endothelium, a second stage of immune antibody-dependent injury of allogenic smooth muscle cells of the media associated with inflammatory infiltration of the adventitia, lastly a third stage of scarring process including intimal proliferation and adventitial fibrosis.

More Related Videos

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis07:05

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis

Published on: May 17, 2015

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Related Concept Videos

Humoral Immune Responses01:36

Humoral Immune Responses

Overview
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...