Related Experiment Video

Updated: Jul 23, 2025

Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition
06:02

Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition

Published on: June 10, 2016

12.3K

TNF superfamily control of tissue remodeling and fibrosis

Hope Steele1,2, Jason Cheng1, Ashley Willicut3

  • 1Division of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.

Frontiers in Immunology
|July 19, 2023
PubMed

Insights

Tumor necrosis super family (TNFSF) members offer new therapeutic targets for fibrosis, a condition marked by excess matrix protein deposition. Targeting TNFSF may improve treatments for fibrotic diseases affecting organs like the lungs, heart, and liver.

Area of Science:

  • Biomedical Science
  • Molecular Biology
  • Pathology

Background:

  • Fibrosis, characterized by excessive extracellular matrix deposition, is a major cause of mortality.
  • Current therapeutic strategies for fibrosis are limited, highlighting the need for novel treatment options.
  • The tumor necrosis super family (TNFSF) is increasingly recognized for its potential in treating fibrotic diseases.

Purpose of the Study:

  • To review the role of select TNFSF members in various fibrotic conditions.
  • To highlight the direct impact of TNFSF on epithelial cells, fibroblasts, and smooth muscle cells.
  • To discuss ongoing clinical trials targeting TNFSF ligands for fibrosis.

Main Methods:

  • Literature review of TNFSF involvement in fibrotic diseases.
  • Analysis of TNFSF interactions with key cellular components in fibrosis.
  • Summary of clinical trial data for anti-TNFSF therapies.

Main Results:

  • TNFSF members play significant roles in the pathogenesis of fibrosis across multiple organs.
  • Direct cellular effects of TNFSF on epithelial, fibroblast, and smooth muscle cells are evident.
  • Clinical trials are actively investigating TNFSF-targeted therapies for fibrotic conditions.

Conclusions:

  • Targeting TNFSF represents a promising therapeutic strategy for managing fibrotic diseases.
  • Combination therapies involving TNFSF modulators may enhance treatment efficacy and selectivity.
  • Further research into TNFSF pathways is crucial for developing effective anti-fibrotic treatments.
Keywords:
TNF superfamilyTNFSFfibrosismucosaremodeling

More Related Videos

Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay11:38

Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

Published on: September 14, 2021

3.4K
Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

7.2K

Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
2.1K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.4K
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
174
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.5K
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
1.1K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.0K