Related Experiment Video
Updated: Dec 7, 2025
06:46
Ex Vivo Corneal Organ Culture Model for Wound Healing Studies
Published on: February 15, 2019
12.3K
TWEAK/Fn14 axis is an important player in fibrosis
Yitian Zhang1, Weihui Zeng1, Yumin Xia1
1Department of Dermatology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Journal of Cellular Physiology
|October 1, 2020
Summary
The TWEAK/Fn14 pathway drives fibrosis by promoting inflammation and myofibroblast activation, contributing to abnormal tissue repair. Targeting this pathway offers therapeutic potential for fibrotic diseases.
Area of Science:
- Cell Biology
- Pathology
- Immunology
Background:
- Fibrosis, a pathological condition of abnormal tissue repair, lacks well-understood etiology and molecular mechanisms.
- Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) are key players in cellular signaling.
- TWEAK/Fn14 signaling exacerbates tissue injury by promoting inflammation and immune responses.
Purpose of the Study:
- To review the molecular mechanisms of TWEAK/Fn14 pathway in fibrosis development and progression.
- To discuss the therapeutic potential of targeting the TWEAK/Fn14 axis in fibrotic diseases.
Main Methods:
- Literature review of experimental evidence.
- Analysis of molecular mechanisms in various cell types and injury models.
- Examination of data from injured and fibrotic tissues.
Main Results:
- TWEAK/Fn14 signaling promotes pro-inflammatory cytokine expression post-injury.
- The TWEAK/Fn14 axis drives myofibroblast activation, proliferation, and extracellular matrix secretion.
- This pathway sustains and perpetuates the fibrotic process.
Conclusions:
- The TWEAK/Fn14 pathway is a critical mediator in the development and progression of fibrosis.
- Modulating the TWEAK/Fn14 pathway presents a promising therapeutic strategy for fibrosis-associated diseases.
Related Concept Videos
01:09Introduction to Fibroblasts
3.6K
Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
3.6K
01:16Clot Retraction and Fibrinolysis
7.9K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
7.9K
00:55Fibrous Proteins
3.9K
Fibrous proteins are either long and narrow proteins or assemble to form long and thin structures. They contain repetitive units and usually consist of either alpha helices or beta sheets and, in rare cases, a mix of both. The amino acids in the primary structure often consist of repeating amino acid sequences. The role of fibrous proteins is primarily structural. Many are located in the extracellular matrix and are present in connective tissues to impart strength and joint mobility. They are...
3.9K
01:16TGF - β Signaling Pathway
9.8K
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...
9.8K
01:25Fibronectins Connect Cells with ECM
3.1K
Fibronectin is an adhesive glycoprotein present in the extracellular matrix of embryogenic and adult tissue. These molecules primarily aid in regulating cell motility and attachment. A fibronectin molecule is composed of two identical polypeptide chains attached to each other by a pair of disulfide bonds at the C-terminal.
Both proteoglycans and collagen are attached to fibronectin proteins, which, in turn, are attached to integrin proteins. These integrin proteins interact with transmembrane...
Both proteoglycans and collagen are attached to fibronectin proteins, which, in turn, are attached to integrin proteins. These integrin proteins interact with transmembrane...
3.1K
01:11Fibril-associated Collagen
3.1K
Fibril-associated collagens are a type of collagens present in the extracellular matrix with interrupted triple helices or FACIT (Fibril-associated collagens interrupted triple-helices). FACIT help connect and attach the collagen fibrils with each other as well as with other proteins of the extracellular matrix.
For example, the type II collagen fibrils in cartilage have covalently bound type IX fibril-associated collagens at regular intervals. Other types of fibril-associated collagens are...
For example, the type II collagen fibrils in cartilage have covalently bound type IX fibril-associated collagens at regular intervals. Other types of fibril-associated collagens are...
3.1K