ReviewJournal of orthopaedic translation2026
Tendon stem/progenitor cells in heterotopic ossification: functional regulation, molecular mechanisms and targeted therapeutic strategies.
Review in Journal of orthopaedic translation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heterotopic ossification (HO) is a pathological process in which ectopic bone tissue forms within soft tissues such as tendons, resulting in pain, limited range of motion, and functional disability that reduces the quality of life. In recent years, tendon stem/progenitor cells (TSPCs) have been considered a key cellular source of HO due to their inherent multilineage differentiation potential. This review aims to systematically elaborate on the advances in the functional regulation and mechanisms of TSPCs in HO. Existing evidence (including lineage tracing and clinical studies) indicates that under the stimulation of trauma, inflammation, and other factors, the chondrogenic and osteogenic differentiation of TSPCs are abnormally activated, shifting their fate from tendon repair to ectopic bone formation. This process is centrally regulated by osteochondrogenesis-related signaling pathways such as BMP, as well as inflammatory signaling pathways such as NF-κB. External factors such as mechanical and inflammatory microenvironment also play important stimulatory roles. Based on these mechanisms, drugs and biomaterials targeting the function of TSPCs have shown potential for the prevention and treatment of HO. Future research needs to explore the heterogeneity of TSPCs and the spatiotemporal dynamics of their regulatory networks, providing theoretical support for the clinical translation of therapeutic strategies. The translational potential of this article: Given the critical role of TSPCs in driving heterotopic ossification through aberrant differentiation, targeting these cells represents a highly promising translational strategy. This review details how external stimuli change the local microenvironment and disrupt the signaling networks within TSPCs, shifting their fate from tissue repair to abnormal bone formation. Highlighting the application of pharmacological agents and biomaterials to precisely modulate the behavior of TSPCs supports a crucial shift toward targeted preventative therapies.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.