ArticleAnais brasileiros de dermatologia
Inhibition of ANGPT2 activates autophagy during hypertrophic scar formation via PI3K/AKT/mTOR pathway.
Article in Anais brasileiros de dermatologia. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- ANGPT2 Drives Thyroid Cancer Progression Through PI3K/AKT Signaling and Correlates With Poor Prognosis and Immune Infiltration.World journal of otorhinolaryngology - head and neck surgery · 2026Article
- Adipose-derived stem cell peptide 5 alleviates hypertrophic scarring through targeting pyruvate carboxylase or p50 to coordinate PI3K/AKT/mTOR-autophagy and NF-κB/IL-6 signaling.Burns & trauma · 2026Article
- Deciphering the cellular landscape of pathological scars.Burns & trauma · 2026Article
- FBXW7 regulates MAP7 through ubiquitination to affect the phenotypic characteristics and paclitaxel sensitivity of paclitaxel-resistant lung adenocarcinoma cells.European journal of medical research · 2025Article
- Downregulation of AKT-mediated p27IBRO neuroscience reports · 2025Article
- Effects of 12 Weeks of Interval Block Resistance Training Versus Circuit Resistance Training on Body Composition, Performance, and Autonomic Recovery in Adults: Randomized Controlled Trial.Journal of functional morphology and kinesiology · 2025Article
- The flavonoid ofFrontiers in pharmacology · 2025Article
- The PI3K/AKT/mTOR pathway in scar remodeling and keloid formation: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2025Review
- Fibroblast PI3K/AKT signaling and extracellular matrix homeostasis: mechanisms, targets, and delivery challenges.Frontiers in cell and developmental biology · 2025Review
- NIR-II light based combinatorial management of hypertrophic scar by inducing autophagy in fibroblasts.Journal of nanobiotechnology · 2024Article
- Natural products for the treatment of hypertrophic scars: Preclinical and clinical studies.Heliyon · 2024Review
- Article
- Silencing ANGPT2 alleviates ulcerative colitis by regulating autophagy-mediated NLRP3 inflammasome inactivation via the mTOR signaling pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- Snail Slime Extracted by a Cruelty Free Method Preserves Viability and Controls Inflammation Occurrence: A Focus on Fibroblasts.Molecules (Basel, Switzerland) · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypertrophic scar (HS), a fibroproliferative disorder caused by aberrant wound healing following skin injuries such as burns, lacerations and surgery, is characterized by invasive proliferation of fibroblasts and excessive extracellular matrix (ECM) accumulation. The dysregulation of autophagy is the pathological basis of HS formation. Previously, angiopoietin-2 (ANGPT2) was found to be overexpressed in HS fibroblasts (HSFs) compared with normal skin fibroblasts. However, whether ANGPT2 participates in the process of HS formation and the potential molecular mechanisms are not clear.
objectiveThis study is intended to figure out the role of ANGPT2 and ANGPT2-mediated autophagy during the development of HS.
methodsRT-qPCR was used to detect ANGPT2 expression in HS tissues and HSFs. HSFs were transfected with sh-ANGPT2 to knock down ANGPT2 expression and then treated with MHT1485, the mTOR agonist. The effects of sh-ANGPT2 or MHT1485 on the proliferation, migration, autophagy and ECM accumulation of HSFs were evaluated by CCK-8 assay, Transwell assay and western blotting. The expression of PI3K/Akt/mTOR pathway-related molecules (p-PI3K, p-Akt and p-mTOR) was assessed by western blotting.
resultsANGPT2 expression was markedly upregulated in HS tissues and HSFs. ANGPT2 knockdown decreased the expression of p-PI3K, p-Akt and p-mTOR. ANGPT2 knockdown activated autophagy and inhibited the proliferation, migration, and ECM accumulation of HSFs. Additionally, the treatment of MHT1485, the mTOR agonist, on ANGPT2-downregulated HSFs, partially reversed the influence of ANGPT2 knockdown on HSFs. STUDY LIMITATIONS: The study lacks the establishment of more stable in vivo animal models of HS for investigating the effects of ANGPT2 on HS formation in experimental animals.
conclusionsANGPT2 downregulation represses growth, migration, and ECM accumulation of HSFs via autophagy activation by suppressing the PI3K/Akt/mTOR pathway. Our study provides a novel potential therapeutic target for HS.
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