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Related Concept Videos

Introduction to Fibroblasts01:09

Introduction to Fibroblasts

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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...
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Clot Retraction and Fibrinolysis01:16

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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.
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Fibrous Proteins00:55

Fibrous Proteins

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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...
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TGF - β Signaling Pathway01:16

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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...
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Role of Matrix Metalloproteases in Degradation of ECM01:23

Role of Matrix Metalloproteases in Degradation of ECM

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Matrix metalloproteases (MMPs) are enzymes involved in the hydrolysis of proteins and glycoproteins of the extracellular matrix. MMPs are essential for the migration and proliferation of cells through the dense matrix network, throughout embryonic development, and throughout morphogenesis. The first MMP activity discovered was a collagenase in a tadpole's tail undergoing metamorphosis. The active collagen deposition and modifications lead to the morphogenesis of tadpoles into the adult...
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Three main types of fibers are secreted by fibroblasts: collagen fibers, elastic fibers, and reticular fibers. Collagen fiber is made from fibrous protein subunits linked together to form a long, straight fiber. Collagen fibers, while flexible, have great tensile strength, resist stretching, and give ligaments and tendons their characteristic resilience and strength. These fibers hold connective tissues together, even during the body's movement.
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Related Experiment Video

Updated: Oct 16, 2025

Ex Vivo Corneal Organ Culture Model for Wound Healing Studies
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TRIM proteins in fibrosis.

Hao Qian1, Lijuan Chen1

  • 1Department of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, Dingjiaqiao 87, Gulou district, Nanjing 210000, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|October 22, 2021
PubMed
Summary

Fibrosis, a result of tissue repair, involves extracellular matrix imbalance. TRIM proteins are increasingly recognized for their role in regulating fibrosis development and progression.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Background:

  • Fibrosis results from disrupted tissue repair and extracellular matrix homeostasis.
  • Excessive extracellular matrix deposition impairs tissue and organ function.
  • Targeting fibrosis mechanisms is a critical research area.

Purpose of the Study:

  • To review recent findings on TRIM proteins in fibrosis regulation.
  • To highlight the role of TRIM proteins in fibrosis-related cytokines and pathways.

Main Methods:

  • Literature review of recent research on TRIM proteins and fibrosis.
  • Analysis of TRIM protein involvement in cellular processes like ubiquitination.
  • Examination of TRIM protein interactions with fibrosis-related signaling pathways.

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Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition
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Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
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Main Results:

  • The TRIM family, an E3 ubiquitin ligase subfamily, plays a significant role in fibrosis.
  • TRIM proteins regulate key biological processes including signal transduction, apoptosis, autophagy, and immunity.
  • Emerging evidence points to TRIM proteins as crucial regulators in the development and progression of fibrosis.

Conclusions:

  • TRIM proteins are pivotal in the complex mechanisms underlying fibrosis.
  • Understanding TRIM protein functions offers potential therapeutic targets for mitigating fibrotic damage.
  • Further research into TRIM proteins and associated pathways is essential for developing anti-fibrotic strategies.