ArticleBioactive materials2026
On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation.
Article in Bioactive materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
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Who cites it
2 citing papers in PubMed.
- Tendon stem/progenitor cells in heterotopic ossification: functional regulation, molecular mechanisms and targeted therapeutic strategies.Journal of orthopaedic translation · 2026Review
- Nanomaterial-Based Photothermal Therapy for Inflammatory Diseases: Intervention Strategies, Synergistic Effects, and Future Challenges.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Achilles tendinopathy represents a prototypical musculoskeletal disorder driven by a self-perpetuating "inflammaging" vicious cycle, where chronic inflammation and stem cell senescence mutually reinforce to precipitate tissue failure. Current therapeutics inadequately address the complex intercellular signaling fueling this loop. Herein, we present a reactive oxygen species (ROS)-responsive photothermal cascade nanoplatform (LT-NPs) that couples Licochalcone A delivery with mild near-infrared (NIR) hyperthermia (∼42 °C). Unlike conventional ablative therapies, this platform leverages mild thermal stress as a safe, generalized immunometabolic modulator. Mechanistically, we identify the mitochondrial DNA (mtDNA)-cGAS-STING axis as the pivotal "bridge" connecting mitochondrial dysfunction to immune dysregulation. The LT-NPs-NIR system dismantles this pathology via a synergistic "dual-lock" strategy: (1) mild photothermal heating induces heat shock protein 70 (HSP70) to seal mtDNA leakage; and (2) released Licochalcone A directly inhibits the downstream STING sensor. Crucially, this intervention re-engineers the dysregulated crosstalk between the immune niche and tendon stroma: by reprogramming M1 macrophages toward a reparative M2 phenotype and simultaneously rescuing tendon stem/progenitor cells (TSPCs) from senescence-associated secretory phenotype (SASP)-mediated senescence, the platform effectively uncouples the reciprocal feedback loop between inflammation and degeneration. In vivo, this orchestrated restoration of the microenvironment significantly suppresses heterotopic ossification and recovers biomechanical function. Consequently, the "mild photothermal cascade" concept establishes a versatile therapeutic paradigm, offering a scalable strategy to resolve the intricate inflammation-senescence crosstalk across a broad spectrum of age-related pathologies.
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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 OpenQuestion graph.