Nieves Elisa B, García Andrés J
Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia, USA.
Petit Institute for Bioengineering and Biosciences, Georgia Institute of Technology, Atlanta, Georgia, USA.
Curr Opin Biomed Eng. 2025 Sep;35. doi: 10.1016/j.cobme.2025.100598. Epub 2025 May 17.
Fibrotic diseases are characterized by the excess production of extracellular matrix components that leads to changes in tissue mechanics and function. Mechanosensing altered during the onset of pulmonary fibrosis is hypothesized to form a positive-feedback loop that contributes to the progression of the disease. However, the exact mechanism(s) leading to fibrotic tissue remodeling as opposed to homeostatic tissue remodeling remains unknown. The development of innovative laboratory models of pulmonary fibrosis has facilitated mechanistic studies of pathogenic mechanosensing and identified new anti-fibrotic candidates. This brief review will cover recent (< 5 years) publications that explore mechanotransduction pathways contributing to the development of pulmonary fibrosis and innovative laboratory models that can advance the field.
纤维化疾病的特征是细胞外基质成分过度产生，导致组织力学和功能发生变化。据推测，肺纤维化发病过程中机械传感的改变会形成一个正反馈回路，促进疾病进展。然而，导致纤维化组织重塑而非稳态组织重塑的确切机制仍然未知。肺纤维化创新实验室模型的发展促进了对致病性机械传感的机制研究，并确定了新的抗纤维化候选物。这篇简短的综述将涵盖最近（<5年）探索促成肺纤维化发展的机械转导途径的出版物以及能够推动该领域发展的创新实验室模型。
