Pulmonary Fibrosis (PF) is generally defined as a specific form of chronic, progressive lung interstitial disease, which is mainly manifested by the abnormal increase of interstitial cells and extracellular matrix in the patient's alveolar area, resulting in thickened alveolar wall, leading to abnormal remodeling of the of lung tissue structure and death of the patient due to respiratory failure. The exposure of alveolar cells to continuously elevated mechanical stress is a key driver of pulmonary fibrosis that begins at the lobe margin and progresses toward the center of the lung, but it's still unclear how these mechanical signals are translated into intracellular chemical signals that lead to cellular behavior.
Recently, the interdisciplinary respiratory disease team of our school published a series of papers entitled ATF3-activated accelerating effect of LINC00941/lncIAPF on fibroblast-to-myofibroblast differentiation by blocking autophagy depending on ELAVL1/HuR in pulmonary fibrosis on Autophagy and hnRNPL-activated circANKRD42 back-splicing and circANKRD42-mediated crosstalk of mechanical stiffness and biochemical signal in lung fibrosis on Molecular Therapy. Through high-throughput sequencing, two non-coding genes, lncIAPF and circANKRD42, were screened and independently named, and lncIAPF and circANKRD42 gain-of-function and loss-of-function fibroblast and mouse models of pulmonary fibrosis were constructed. Based on samples of patients with pulmonary fibrosis, the role and mechanism of mechanical stress, such as cytoskeleton allosteric and matrix stiffness, in the evolution of pulmonary fibrosis are systematically explained, from the perspective of non-coding genes, providing candidate genes for gene/drug therapy and diagnostic markers of pulmonary fibrosis.
Zhang Jinjin, a senior experimenter at the Pharmaceutical Research Center, and Xu Pan, an attending physician in the Department of Respiratory Medicine, Binzhou Affiliated Hospital, are the first authors of the article. Three graduate students, Chen Hongbin, Wang Haixia and Wang Meirong, are the co-authors of the article.
Article Link:
https://www.tandfonline.com/doi/full/10.1080/15548627.2022.2046448
https://pubmed.ncbi.nlm.nih.gov/35278674/
