Related Experiment Video
Updated: Oct 12, 2025
Author Spotlight: Advancing Tendon Research by Developing Mouse Assembloids to Understand Cellular Mechanisms
Published on: March 22, 2024
CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix
Yongsik Cho1,2, Hyeon-Seop Kim1,2, Donghyun Kang1,2
1Center for RNA Research, Institute for Basic Science, 08826 Seoul, South Korea.
Abstract:
Tendinopathy, the most common disorder affecting tendons, is characterized by chronic disorganization of the tendon matrix, which leads to tendon tear and rupture. The goal was to identify a rational molecular target whose blockade can serve as a potential therapeutic intervention for tendinopathy. We identified C1q/TNF-related protein-3 (CTRP3) as a markedly up-regulated cytokine in human and rodent tendinopathy. Overexpression of CTRP3 enhanced the progression of tendinopathy by accumulating cartilaginous proteoglycans and degenerating collagenous fibers in the mouse tendon, whereas CTRP3 knockdown suppressed the tendinopathy pathogenesis. Functional blockade of CTRP3 using a neutralizing antibody ameliorated overuse-induced tendinopathy of the Achilles and rotator cuff tendons. Mechanistically, CTRP3 elicited a transcriptomic pattern that stimulates abnormal differentiation of tendon stem/progenitor cells and ectopic chondrification as an effect linked to activation of Akt signaling. Collectively, we reveal an essential role for CTRP3 in tendinopathy and propose a potential therapeutic strategy for the treatment of tendinopathy.
Insights
Researchers identified C1q/TNF-related protein-3 (CTRP3) as a key driver of tendinopathy. Blocking CTRP3 with an antibody successfully treated tendon injuries, offering a new therapeutic approach for this common disorder.
Area of Science:
- Biochemistry
- Molecular Biology
- Orthopedics
Background:
- Tendinopathy is a prevalent tendon disorder marked by matrix disorganization, often leading to tears and rupture.
- Identifying specific molecular targets is crucial for developing effective therapeutic interventions for tendinopathy.
Purpose of the Study:
- To identify a molecular target for therapeutic intervention in tendinopathy.
- To investigate the role of C1q/TNF-related protein-3 (CTRP3) in tendinopathy pathogenesis.
Main Methods:
- Identified CTRP3 as upregulated in human and rodent tendinopathy models.
- Utilized CTRP3 overexpression and knockdown in mouse tendons.
- Administered a neutralizing antibody against CTRP3 to treat overuse-induced tendinopathy.
Main Results:
- CTRP3 overexpression exacerbated tendinopathy, increasing proteoglycans and degenerating collagen.
- CTRP3 knockdown suppressed tendinopathy progression.
- Antibody blockade of CTRP3 ameliorated Achilles and rotator cuff tendinopathy.
- CTRP3 promoted abnormal stem cell differentiation and chondrification via Akt signaling.
Conclusions:
- CTRP3 plays a critical role in the pathogenesis of tendinopathy.
- Functional blockade of CTRP3 presents a promising therapeutic strategy for treating tendinopathy.
Related Concept Videos
01:24T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
01:21Repressible Operon: trp Operon
01:16TGF - β Signaling Pathway