ReviewFrontiers in pharmacology2025
The PI3K/AKT/mTOR pathway in scar remodeling and keloid formation: mechanisms and therapeutic perspectives.
Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
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.
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Who cites it
9 citing papers in PubMed.
- An adhesive hydrogel enabling spatiotemporal delivery of umbilical cord exosomes for scarless skin regeneration through immunomodulation and ECM remodeling.Bioactive materials · 2027Article
- Wound Healing Potential of Multifunctional Nanomaterials: Mechanism, Future Prospects, and Challenges.Pharmaceutics · 2026Review
- Advanced Functional Wound Dressings in Precision Surgery: Immunometabolic Reprogramming, Bioadaptive Biomaterials, and Intelligent Regenerative Interfaces.International journal of molecular sciences · 2026Review
- The Piezo1-Ca2+-PI3k/Akt signaling axis as a context-dependent mechanotransduction node during skin wound healing.iScience · 2026Review
- Cellular Senescence in Keloid Pathology: Mechanisms, Biomarkers, and Potential Therapeutic Targets.Biomedicines · 2026Review
- Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.Frontiers in immunology · 2026Review
- Single-cell transcriptomic profiling identifies YY1 as a key regulator of fibroblast plasticity in hypertrophic scar formation.Burns & trauma · 2026Article
- Exploring hub genes related to adipocytokines in keloids: a combined analysis integrating single-cell, Mendelian randomization and bulk transcriptome data with experimental verification.Frontiers in molecular biosciences · 2026Article
- Fisetin promotes skin wound healing and inhibits pathological scar formation through modulation of the PI3K/Akt/TGF-β1 signaling axis.Frontiers in pharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloids and hypertrophic scars (HTS) represent aberrant wound healing characterized by excessive fibroblast activity and extracellular matrix accumulation. The PI3K/AKT/mTOR signaling pathway is vital in regulating these processes, promoting fibroblast proliferation, survival, and collagen synthesis. Dysregulation of this pathway, driven by genetic mutations, post-transcriptional modulation, and upstream signaling, contributes significantly to the pathogenesis of pathological scarring. This review collects current knowledge on the molecular mechanisms underlying PI3K/AKT/mTOR activation in keloids and HTS, highlighting the roles of key regulators such as PTEN, NEDD4, and non-coding RNAs. It also evaluates therapeutic strategies targeting this axis, including small-molecule inhibitors, natural compounds, and emerging delivery platforms. Targeting PI3K/AKT/mTOR offers a compelling avenue for developing effective, mechanism-based keloid and hypertrophic scarring treatments. The PI3K/AKT/mTOR signaling axis is central to these cellular mechanisms, which drive fibroblast proliferation, survival, myofibroblast transdifferentiation, and metabolic reprogramming (including suppressed autophagy and enhanced glycolysis.
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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.