ArticleMolecular biology reports2021
M2-polarized macrophages mediate wound healing by regulating connective tissue growth factor via AKT, ERK1/2, and STAT3 signaling pathways.
Article in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 63 citations in OpenAlex.
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- The role of macrophage polarization in organ transplantation: research progress on impact on graft injury, repair, and fibrosis.Frontiers in immunology · 2026Review
- Wounds and the Microbiota: The Healing Interplay Between Host and Microbial Communities.International journal of molecular sciences · 2025Review
- Development of a Collagen-Cerium Oxide Nanohydrogel for Wound Healing: In Vitro and In Vivo Evaluation.Biomedicines · 2025Article
- Lymph node transcriptomic profiles suggest susceptibility to bleomycin-induced pulmonary toxicity in classic hodgkin lymphoma.Scientific reports · 2025Article
- Dysfunctional crosstalk between macrophages and fibroblasts under LPS-infected and hyperglycemic environment in diabetic wounds.Scientific reports · 2025Article
- Macrophage Proangiogenic VEGF-A Is Required for Inflammatory Arteriogenesis During Vascular Injury.Biomedicines · 2025Article
- CD206 and dust particles are prognostic biomarkers of progressive fibrosing interstitial lung disease associated with air pollutant exposure.Scientific reports · 2025Article
- aFGF gene-modified adipose-derived mesenchymal stem cells promote healing of full-thickness skin defects in diabetic rats.Stem cell research & therapy · 2025Article
- The role of natural products targeting macrophage polarization in sepsis-induced lung injury.Chinese medicine · 2025Review
- Biomimetic optimization of silicone breast implant integration: insights into wound healing and the foreign body response.Frontiers in bioengineering and biotechnology · 2025Review
- Yap Is a Nutrient Sensor Sensitive to the Amino Acid L-Isoleucine and Regulates the Expression of Ctgf in Cardiomyocytes.Biomolecules · 2024Article
- Review
- Persistence of lung structural and functional alterations at one year post-COVID-19 is associated with increased serum PD-L2 levels and altered CD4/CD8 ratio.Immunity, inflammation and disease · 2024Article
- LINC00330/CCL2 axis-mediated ESCC TAM reprogramming affects tumor progression.Cellular & molecular biology letters · 2024Article
- Emerging roles of lactate in acute and chronic inflammation.Cell communication and signaling : CCS · 2024Review
- Human Fibroblast-Derived Matrix Hydrogel Accelerates Regenerative Wound Remodeling Through the Interactions with Macrophages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
Corrections and comments
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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
backgroundTimely and sufficient M1 recruitment and M2 polarization are necessary for fibrosis during wound healing. The mechanism of how M2 mediates wound healing is worth exploring. Abnormally up-regulated connective tissue growth factor (CTGF) influences multiple organ fibrosis, including cardiac, pulmonary, hepatic, renal, and cutaneous fibrosis. Previous studies reported that M2 contributed to hepatic and renal fibrosis by secreting CTGF. It is worth discussing if M2 regulates fibrosis through secreting CTGF in wound healing. METHODS AND
resultsWe established the murine wound model and inhibited macrophages during proliferation phase with clodronate liposomes in vivo. Macrophages depletion led to down-regulation of wound healing rates, collagen deposition, as well as expression of collagen 1/3 and Ki67. M2 was induced by interleukin-4 (IL-4) and measured by flow cytometry in vitro. Secreted pro-fibrotic and anti-fibrotic factors were tested by enzyme-linked immunosorbent assay (ELISA). M2 was polarized, which producing more CTGF, transforming growth factor-beta1 (TGF-β1), and IL-6, as well as less tumor necrosis factor-α (TNF-α) and IL-10. M2 CTGF gene was blocked using siCTGF. Effects of M2 on fibroblasts activities were detected by cell counting kit 8 (CCK8) and cellular wound healing assay. Expressions of related signaling pathway were assessed by western blotting. Blockade of CTGF in M2 deactivated fibroblasts proliferation and migration by regulating AKT, ERK1/2, and STAT3 pathway. Recombinant CTGF restored these effects.
conclusionsOur research, for the first time, indicated that M2 promoted wound healing by secreting CTGF, which further mediating proliferation and migration of fibroblasts via AKT, ERK1/2, and STAT3 pathway.
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