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To test the hypothesis that dysregulated wound healing is associated with Urogynecologic mesh complications, we collected vaginal cell secretions using vaginal swabs after polypropylene mesh implantation in patients with (N = 39) and without (N = 40) complication. A customized multiplex immunoassay measured markers of inflammation (MCP-1, IGFBP-1, IL-2, IL-10, IL-17, PDGF-BB, bFGF, IL-1b, IL-6, IL-12p70, TNF-α), neuroinflammation (IL-1RA, TGF-β, IL-15, IL-18, IL-3, M-CSF), angiogenesis (VEGF), and matrix proteins (fibronectin, tenasin c, thrombospondin-2, lumican) between groups. Patients with complications were younger, heavier, implanted with mesh longer, and more likely to be ever smokers. A 5 kg/m BMI increase and ever-smoking were associated with a 2.4-fold and sixfold increased risk of complication, respectively. Patients with the highest tertile of bFGF, fibronectin, thrombospondin-2, TNF-β, or VEGF had an odds ratio (OR) of 11.8 for having a mesh complication while ≥ 3 elevated had an OR of 237 while controlling for age, BMI, and smoking. The highest tertile of bFGF, thrombospondin-2, and fibronectin together perfectly indicated a complication (P < 0.0001). A receiver-operator curve for high bFGF, thrombospondin-2, and fibronectin showed excellent discrimination between complications and controls (AUC 0.87). These data provide evidence of dysregulated wound healing in mesh complications. Modifiable factors provide potential targets for patient counseling and interventions.
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http://dx.doi.org/10.1038/s41598-023-48388-8 | DOI Listing |
Cell Mol Biol (Noisy-le-grand)
September 2025
Arencibia Clinic, San Sebastian, Spain.
Follicular unit extraction (FUE) has become a leading technique in hair transplantation, yet optimal management of the donor area remains a clinical challenge. This systematic review analyzes intraoperative and postoperative interventions applied to the donor area in FUE hair transplantation, with a focus on both clinical outcomes and the cellular and molecular mechanisms involved in tissue repair, inflammatory response, and regenerative processes. A comprehensive literature search was conducted in PubMed and EMBASE (January 2000-June 2025), identifying clinical studies that evaluated donor area treatments and reported outcomes related to healing, inflammation, infection, and patient satisfaction.
View Article and Find Full Text PDFOpen Life Sci
September 2025
Shanghai TCM-Integrated Hospital, Department of Vascular Diseases, Shanghai University of TCM, No. 230, Baoding Road, Hongkou District, Shanghai, Shanghai Municipality, 200082, China.
Wound healing is a precisely regulated dynamic process in which signaling pathways play a central role. This article provides a comprehensive review of the signaling pathways involved in wound healing, emphasizing their roles in inflammation, vascular regeneration, cell proliferation, and extracellular matrix remodeling. We further discuss the crosstalk between these pathways and their contributions to wound healing dysregulation.
View Article and Find Full Text PDFOpen Life Sci
August 2025
Department of Radiology, Xianning Central Hospital, The First Affiliated Hospital of Hubei University of Science and Technology, No. 228, Jingui Road, Xian'an District, Xianning, Hubei, 437000, China.
Peripheral nerve injury-induced muscle atrophy is characterized by chronic inflammation and dysregulated macrophage polarization. RUNX1, a transcription factor upregulated in denervated muscle, has been implicated in linking muscle degeneration to inflammatory processes, but its downstream targets and mechanisms remain unclear. The aim of this study is to delineate the RUNX1-JUNB-NF-κB axis in driving inflammation-mediated muscle atrophy.
View Article and Find Full Text PDFJ Invest Dermatol
September 2025
Department of Surgery, University of California San Diego, La Jolla, CA, United States; Department of Dermatology, University of California San Diego, La Jolla, CA, United States. Electronic address:
Normal cutaneous wound healing is a multicellular process that involves the release of small extracellular vesicles (sEVs) that coordinate intercellular communication by delivery of sEV payloads to recipient cells. We have recently shown how the pro-reparative activity of inflammatory cell sEVs, especially macrophage and neutrophil-derived sEVs, in the wound bed is dysregulated in impaired wound healing. Here we show that loss of Rab27A, a small GTPase that has a regulatory function in sEV secretion, reduces the release of neutrophil and macrophage-derived sEVs.
View Article and Find Full Text PDFInt J Mol Med
November 2025
Department of Anesthesiology, Chongqing Traditional Chinese Medicine Hospital, Chongqing 400021, P.R. China.
Doxorubicin (DOX)‑induced cardiotoxicity (DIC) remains a critical challenge in cancer therapy, significantly limiting its use in clinical practice. The underlying mechanisms involve disruptions in cardiac metabolism and mitochondrial dysfunction. The heart relies on mitochondrial oxidative phosphorylation to produce ATP, which is essential for maintaining both contraction and relaxation.
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