Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis DOI
Tianming Zhao, Yunchao Su

Deleted Journal, Journal Year: 2025, Volume and Issue: 2(1), P. 10001 - 10001

Published: Jan. 1, 2025

Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible, and fatal disease with an increasing incidence limited therapeutic options. It characterized by the formation deposition of excess extracellular matrix proteins resulting in gradual replacement normal lung architecture fibrous tissue. The cellular molecular mechanism IPF has not been fully understood. A hallmark fibroblast to myofibroblast transformation (FMT). During excessive repair upon exposure harmful stimuli, fibroblasts transform into myofibroblasts under stimulation cytokines, chemokines, vesicles from various cells. These mediators interact fibroblasts, initiating multiple signaling cascades, such as TGFβ1, MAPK, Wnt/β-catenin, NF-κB, AMPK, endoplasmic reticulum stress, autophagy, contributing FMT. Furthermore, single-cell transcriptomic analysis revealed significant heterogeneity among myofibroblasts, which arise cell types are adapted altered microenvironment during pathological repair. This review provides overview recent research on origins pathways driving their formation, focus interactions between epithelial cells, endothelial macrophages context fibrosis. Based these insights, targeting FMT could offer promising avenues for treatment IPF.

Language: Английский

Epigenetic Control of Alveolar Macrophages: Impact on Lung Health and Disease DOI Creative Commons
Nirmal Parajuli, Kalpana Subedi, Xzaviar Kaymar Solone

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(9), P. 640 - 640

Published: April 25, 2025

Alveolar macrophages (AMs) are immune cells located in the alveoli-the tiny air sacs lungs where gas exchange occurs. Their functions regulated by various epigenetic mechanisms, which essential for both healthy lung function and disease development. In lung's microenvironment, AMs play critical roles surveillance, pathogen clearance, tissue repair. This review examines how regulation influences AM their involvement diseases. Key such as DNA methylation, histone modifications, non-coding RNAs, regulate gene expression response to environmental signals. lungs, these modifications enable quickly respond inhaled threats. However, when processes malfunction, they could contribute diseases pulmonary fibrosis, COPD, hypertension. By exploring changes affect polarization, plasticity, responses, we can gain deeper insights into role open new avenues treating preventing respiratory conditions. Ultimately, understanding mechanisms within enhances our knowledge of immunology offers potential innovative interventions restore health prevent

Language: Английский

Citations

0

Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis DOI
Tianming Zhao, Yunchao Su

Deleted Journal, Journal Year: 2025, Volume and Issue: 2(1), P. 10001 - 10001

Published: Jan. 1, 2025

Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible, and fatal disease with an increasing incidence limited therapeutic options. It characterized by the formation deposition of excess extracellular matrix proteins resulting in gradual replacement normal lung architecture fibrous tissue. The cellular molecular mechanism IPF has not been fully understood. A hallmark fibroblast to myofibroblast transformation (FMT). During excessive repair upon exposure harmful stimuli, fibroblasts transform into myofibroblasts under stimulation cytokines, chemokines, vesicles from various cells. These mediators interact fibroblasts, initiating multiple signaling cascades, such as TGFβ1, MAPK, Wnt/β-catenin, NF-κB, AMPK, endoplasmic reticulum stress, autophagy, contributing FMT. Furthermore, single-cell transcriptomic analysis revealed significant heterogeneity among myofibroblasts, which arise cell types are adapted altered microenvironment during pathological repair. This review provides overview recent research on origins pathways driving their formation, focus interactions between epithelial cells, endothelial macrophages context fibrosis. Based these insights, targeting FMT could offer promising avenues for treatment IPF.

Language: Английский

Citations

0