Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cell-mediated Immune Responses01:40

Cell-mediated Immune Responses

Overview
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...
Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
Tissue Transplantation01:24

Tissue Transplantation

Tissue transplantation is a significant medical procedure involving the transfer of cells, tissues, or organs from a donor to a recipient, with the primary aim of restoring lost functions. This procedure is crucial in treating a broad spectrum of diseases, including kidney diseases, liver failure, heart disease, and certain types of cancers.
The Biology of Tissue Transplantation
The biology of tissue transplantation hinges on the Major Histocompatibility Complex (MHC) molecules. These molecules...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...
Diabetic Retinopathy01:27

Diabetic Retinopathy

DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Power and sample-size estimation in human microbiome research.

Med (New York, N.Y.)·2026
Same author

Hypoxia Induces Adaptive Lymphangiogenesis via Cd74 and Vegfr3 to Modulate Pulmonary Hypertension.

Circulation research·2026
Same author

CES1 deficiency is associated with metabolic reprograming and endothelial dysfunction in pulmonary arterial hypertension.

American journal of respiratory and critical care medicine·2026
Same author

Pumping Up Dermatologic Drug Reformulation: A Review of How Proton Pump Inhibitors May Revolutionize Scleroderma Treatment.

The Journal of clinical and aesthetic dermatology·2026
Same author

Esomeprazole inhibits proliferation of scleroderma fibroblasts via cell cycle regulation.

Frontiers in pharmacology·2026
Same author

Correction to: Ultrasound Neuromodulation of an Anti-Inflammatory Pathway at the Spleen Improves Experimental Pulmonary Hypertension.

Circulation research·2026

Related Experiment Video

Updated: May 14, 2026

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
07:05

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis

Published on: May 17, 2015

Complement-mediated microvascular injury leads to chronic rejection.

Mohammad A Khan1, Mark R Nicolls

  • 1Division of Pulmonary and Critical Care Medicine, Department of Medicine, VA Palo Alto/Stanford University School of Medicine, 300 Pasteur Dr A283 MC 5351, Stanford, CA 94305, USA.

Advances in Experimental Medicine and Biology
|February 14, 2013
PubMed
Summary

Microvascular loss drives chronic lung transplant rejection. Targeting complement pathways can prevent this, improving graft survival and preventing airway fibrosis, known as bronchiolitis obliterans syndrome.

Related Experiment Videos

Last Updated: May 14, 2026

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
07:05

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis

Published on: May 17, 2015

Area of Science:

  • Transplantation immunology
  • Vascular biology
  • Organ rejection mechanisms

Background:

  • Microvascular loss is a key factor in chronic rejection across solid organ transplants.
  • Lung transplants are particularly susceptible due to their reliance on microcirculation establishment post-surgery.
  • This microvascular damage can lead to ischemia, tissue infarction, and airway fibrosis, collectively termed bronchiolitis obliterans syndrome (BOS).

Purpose of the Study:

  • To investigate the role of the complement system in acute microvascular loss and ischemia during lung transplant rejection.
  • To evaluate the impact of complement inhibition on preventing airway fibrosis and promoting vascular repair in lung allografts.

Main Methods:

  • Utilized a mouse orthotopic tracheal transplantation model to study airway vasculature rejection.
  • Monitored C3 deposition on vascular endothelium and tissue hypoxia.
  • Assessed the effects of complement deficiency and inhibition on graft oxygenation, airway remodeling, and vascular repair.
  • Investigated the roles of CD4+ T cells and antibody-dependent complement activity in vascular destruction.

Main Results:

  • C3 complement deposits were observed on vascular endothelium preceding airway fibrosis and coinciding with initial tissue hypoxia.
  • Microvascular blood flow cessation occurred during graft rejection.
  • Complement deficiency and inhibition significantly improved tissue oxygenation, reduced airway remodeling, and accelerated vascular repair.
  • Both CD4+ T cells and antibody-dependent complement activity were found to independently cause vascular destruction and ischemia.

Conclusions:

  • Complement activation is a critical mediator of microvascular injury and ischemia in acute lung transplant rejection.
  • Targeting complement-mediated microvascular damage, alongside standard immunosuppression, may prevent chronic rejection and bronchiolitis obliterans syndrome.
  • Maintaining vascular health in lung allografts is crucial for long-term transplant success.