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

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Autoimmune Disorders01:29

Autoimmune Disorders

Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune system...
Overview of Systemic Arteries01:11

Overview of Systemic Arteries

The human body is a complex, well-organized machine, and at the heart of its operations lies the circulatory system. This network of blood vessels, which includes systemic arteries, plays a vital role in maintaining life by transporting nutrients, oxygen, and waste products to and from cells throughout the body.
Systemic circulation is the part of the cardiovascular system that carries oxygenated blood away from the heart to the body's tissues and returns deoxygenated blood back to the heart.
Rheumatic Heart Disease I: Introduction01:23

Rheumatic Heart Disease I: Introduction

Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...

You might also read

Related Articles

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

Sort by
Same author

Multicytokine-based transcriptome-wide association study for 7 inflammatory skin disorders identifies candidate causal genes in keratinocytes.

The Journal of allergy and clinical immunology·2026
Same author

Imbalance of Ciliary Programs Drives Fibroblast Differentiation and Fibrotic Signaling in Systemic Sclerosis.

bioRxiv : the preprint server for biology·2026
Same author

Aurora A kinase activation contributes to the fibrotic phenotype in systemic sclerosis through primary cilia shortening.

Arthritis research & therapy·2026
Same author

Nintedanib attenuates profibrotic gene expression in a 3-dimensional organotypic culture model of systemic sclerosis skin fibrosis.

The Journal of investigative dermatology·2026
Same author

A potent inhibitor of PAI-1, MDI-2517, mitigates disease severity in a preclinical systemic sclerosis model.

JCI insight·2026
Same author

Gain of function NOTCH4 variants disrupt angiogenesis in systemic sclerosis.

Annals of the rheumatic diseases·2026
Same journal

Mosaicplasty for the treatment of the osteochondral lesion in the femoral head.

Bulletin of the NYU hospital for joint diseases·2012
Same journal

Hibernoma--a case series with multimodality imaging and pathologic correlation.

Bulletin of the NYU hospital for joint diseases·2012
Same journal

Progressive migration of broken Kirschner wire into the proximal tibia following tension-band wiring technique of a patellar fracture--case report.

Bulletin of the NYU hospital for joint diseases·2012
Same journal

Multidrug-resistant Acinetobacter baumannii infection following para-articular steroid injection in the knee--a case report.

Bulletin of the NYU hospital for joint diseases·2012
Same journal

Extensor indicis proprius and extensor digitorum communis rupture after volar locked plating of the distal radius--a case report.

Bulletin of the NYU hospital for joint diseases·2012
Same journal

Bilateral four-part anterior fracture dislocation of the shoulder--a case report and review of literature.

Bulletin of the NYU hospital for joint diseases·2012
See all related articles

Related Experiment Video

Updated: Jun 28, 2026

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease
04:44

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Published on: June 16, 2020

Systemic sclerosis: an update.

John Varga1

  • 1Northwest University, Feinberg School of Medicine, Chicago, Illinois, USA. j-varga@northwestern.edu

Bulletin of the NYU Hospital for Joint Diseases
|October 22, 2008
PubMed
Summary
This summary is machine-generated.

Systemic sclerosis (SSc) is a complex autoimmune disease. Targeting transforming growth factor-beta (TGF-β) may offer new therapeutic strategies for inhibiting fibrosis in SSc patients.

More Related Videos

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

Related Experiment Videos

Last Updated: Jun 28, 2026

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease
04:44

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Published on: June 16, 2020

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

Area of Science:

  • Immunology
  • Rheumatology
  • Fibrosis Research

Background:

  • Systemic sclerosis (SSc) is a chronic autoimmune disease with high variability in patient outcomes.
  • Pathogenesis involves vascular, immune, and fibrotic processes, complicating treatment.
  • Current non-selective therapies for SSc have limited disease-modifying effects.

Purpose of the Study:

  • To explore novel therapeutic targets for Systemic Sclerosis.
  • To investigate the role of transforming growth factor-beta (TGF-β) in SSc pathogenesis.
  • To evaluate the potential of TGF-β inhibitors for treating SSc-related fibrosis.

Main Methods:

  • Review of current understanding of SSc pathogenesis.
  • Analysis of the role of TGF-β signaling in fibroblast activation and collagen production.
  • Discussion of emerging TGF-β targeted therapies, including neutralizing antibodies and small molecules.

Main Results:

  • Transforming growth factor-beta (TGF-β) is implicated in fibroblast activation and excessive collagen deposition in SSc.
  • Vascular interventions can reduce SSc complications, but immune-targeted therapies are often non-selective.
  • TGF-β signaling blockade shows promise in selectively inhibiting fibrosis progression.

Conclusions:

  • Novel therapeutic strategies for SSc should address autoimmunity, vascular injury, and fibrosis.
  • Targeting TGF-β signaling represents a promising approach for developing disease-modifying therapies for Systemic Sclerosis.
  • TGF-β inhibitors are advancing towards clinical trials for SSc treatment.