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Keloids are scars that grow abnormally due to excessive extracellular matrix production by fibroblasts and increased angiogenesis. Chronic tension is implicated in their growth, but the exact pathology remains unclear. This study investigated the increased expression of molecules responsible for sensing pressure in keloids compared with lymphedema, which is also a non-tumorous fibroproliferative disease caused by another etiology. Higher expression levels of COL1A2, PIEZO2, and POSTN were observed in the keloid group compared with the lymphedema group. PIEZO2 expression levels showed a strong correlation with both COL1A2 (r = 0.9252, 95% CI 0.8474-0.9641, p < 0.001) and POSTN (r = 0.9118, 95% CI 0.8213-0.9575, p < 0.001). Additionally, PIEZO2 expression levels were significantly higher in recurrent keloids than in non-recurrent keloids (3,032.5 ± 1,090.2 versus 1,241.9 ± 860.7, p = 0.032). Analysis of gene expression at the single-cell level found upregulation of PIEZO2 in vascular and lymphatic endothelial cells, and a subgroup of fibroblasts. Additionally, COL1A1, COL1A2, COL3A1, and POSTN expression was also increased in the fibroblast subgroup. Furthermore, in fibroblasts with high PIEZO2 expression, extracellular matrix collagen production signaling was augmented. Histological analysis confirmed the presence of PIEZO2-positive cells in the perivascular stroma active area of keloid tissue, together with inflammatory cells. Therefore, since PIEZO2-positive cells are highly expressed specifically in keloids and are deeply involved in their recurrence and activity, we propose that the pathogenesis of keloids is constructed by PIEZO2-positive cells. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.
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http://dx.doi.org/10.1002/path.6455 | DOI Listing |
Int J Gen Med
September 2025
Department of Geriatrics, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, People's Republic of China.
Background: Sepsis is characterized by profound immune and metabolic perturbations, with glycolysis serving as a pivotal modulator of immune responses. However, the molecular mechanisms linking glycolytic reprogramming to immune dysfunction remain poorly defined.
Methods: Transcriptomic profiles of sepsis were obtained from the Gene Expression Omnibus.
Mol Ther Methods Clin Dev
June 2025
Université Paris-Saclay, University Evry, Inserm, Genethon, Integrare Research Unit UMR_S951, 91000 Evry, France.
Pompe disease is a glycogen storage disorder caused by mutations in the acid α-glucosidase (GAA) gene, leading to reduced GAA activity and glycogen accumulation in heart and skeletal muscles. Enzyme replacement therapy with recombinant GAA, the standard of care for Pompe disease, is limited by poor skeletal muscle distribution and immune responses after repeated administrations. The expression of GAA in muscle with adeno-associated virus (AAV) vectors has shown limitations, mainly the low targeting efficiency and immune responses to the transgene.
View Article and Find Full Text PDFResearch (Wash D C)
September 2025
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype, characterized by a high propensity for metastasis, poor prognosis, and limited treatment options. Research has demonstrated a substantial correlation between the expression of protein arginine N-methyltransferase 1 (PRMT1) and enhanced proliferation, metastasis, and poor outcomes in TNBC. However, the specific role of PRMT1 in lung metastasis and chemoresistance remains unclear.
View Article and Find Full Text PDFFront Immunol
September 2025
Institute of Pulmonary Medicine, Hadassah Hebrew University Medical Center, Jerusalem, Israel.
Neutrophil extracellular traps (NETs) are DNA-protein structures released during a form of programmed neutrophil death known as NETosis. While NETs have been implicated in both tumor inhibition and promotion, their functional role in cancer remains ambiguous. In this study, we compared the NET-forming capacity and functional effects of NETs derived from lung cancer (LC) patients and healthy donors (H).
View Article and Find Full Text PDFFront Immunol
September 2025
Department of Thoracic Surgery, Shenzhen People's Hospital (The First Affiliated Hospital, Southern University of Science and Technology; The Second Clinical Medical College, Jinan University), Shenzhen, Guangdong, China.
Background: Lung cancer remains the leading cause of cancer-related mortality globally, primarily due to late-stage diagnosis, molecular heterogeneity, and therapy resistance. Key biomarkers such as EGFR, ALK, KRAS, and PD-1 have revolutionized precision oncology; however, comprehensive structural and clinical validation of these targets is crucial to enhance therapeutic efficacy.
Methods: Protein sequences for EGFR, ALK, KRAS, and PD-1 were retrieved from UniProt and modeled using SWISS-MODEL to generate high-confidence 3D structures.