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Home
Engineered Nestin+ Tspc-derived Exosomes Promote Tendon Repair Via Metabolic Reprogramming.

Home
Engineered Nestin+ Tspc-derived Exosomes Promote Tendon Repair Via Metabolic Reprogramming.

Related Experiment Video

Engineering Tendon Assembloids to Probe Cellular Crosstalk in Disease and Repair

Engineering Tendon Assembloids to Probe Cellular Crosstalk in Disease and Repair

Published on: March 22, 2024

Engineered Nestin⁺ TSPC-Derived Exosomes Promote Tendon Repair Via Metabolic Reprogramming.

Linxiang Cheng^1,2,3,4,5, Junyu Guo^6,2,3,4, Junshu Zhang^6,2,3,4

¹Department of Orthopedic Surgery of Sir Run Run Shaw Hospital, and Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, PR China.

Journal of Extracellular Vesicles

|June 17, 2026

View abstract on PubMed

Summary

This summary is machine-generated.

Engineered exosomes from Nestin-overexpressing tendon stem/progenitor cells (Nes-EVs) effectively treat tendinopathy. These Nes-EVs reduce cell aging and restore tendon function by enhancing mitochondrial metabolism.

Keywords:

engineered TSPC exosomes nestin tendinopathy

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Published on: August 1, 2020

Area of Science:

Regenerative Medicine
Cell Biology
Biochemistry

Background:

Tendon repair is a significant clinical challenge with few effective treatments.
Nestin-positive tendon stem/progenitor cells (TSPCs) are crucial for tendon healing but face clinical translation hurdles.

Purpose of the Study:

To investigate the therapeutic potential of exosomes derived from engineered Nestin-overexpressing TSPCs (Nes-EVs) for tendinopathy.
To elucidate the underlying mechanisms by which Nes-EVs promote tendon healing.

Main Methods:

Lentiviral Nestin overexpression in TSPCs to generate Nes-EVs.
In vitro assessment of Nes-EVs' effects on cellular senescence and tenogenic differentiation.
In vivo evaluation of Nes-EVs in collagenase-induced and aged murine tendinopathy models.

Integrated transcriptomic and metabolomic profiling of TSPCs and Nes-EVs.

Main Results:

Nes-EVs significantly improved motor function, tissue architecture, and collagen homeostasis in tendinopathy models.
Nes-EVs reduced senescence markers and promoted tenogenic differentiation in vitro.
Transcriptomic and metabolomic analyses revealed enrichment in pantothenate and CoA biosynthesis.
Nes-EVs enhanced tenocyte mitochondrial function, boosting ATP production and reducing oxidative stress.

Conclusions:

Nes-EVs represent a promising acellular therapeutic strategy for tendinopathy.
Nes-EVs coordinate tendon metabolism and homeostasis, offering a novel treatment approach.
Targeting cellular metabolism via Nes-EVs revitalizes damaged tendons.