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Cited by 212 publications
(190 citation statements)
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“…In this issue of the Journal , Yao and colleagues (pp. 707–717 ) have developed a new mouse model of pulmonary fibrosis, induced by genetic Sin3a loss of function (Sin3a-LOF) in alveolar type 2 (AT2) cells ( 1 ). Unlike the single-dose bleomycin model of fibrosis, in which fibrosis peaks 21 days after exposure and then largely resolves, the fibrosis in Sin3a-LOF mice progresses steadily over 4–8 weeks, eventually causing death.…”
mentioning
confidence: 99%
“…In this issue of the Journal , Yao and colleagues (pp. 707–717 ) have developed a new mouse model of pulmonary fibrosis, induced by genetic Sin3a loss of function (Sin3a-LOF) in alveolar type 2 (AT2) cells ( 1 ). Unlike the single-dose bleomycin model of fibrosis, in which fibrosis peaks 21 days after exposure and then largely resolves, the fibrosis in Sin3a-LOF mice progresses steadily over 4–8 weeks, eventually causing death.…”
mentioning
confidence: 99%
“…AT2 cells are a primary target of injury in IPF, and the processes involved in AT2 cellular senescence and in ammation are crucial for the development of brotic lung disease [21][22][23][24][25]. Moreover, the LINE TE family, particularly the upregulation of the autonomous (expressed from intergenic region, i.e., not from genic region and thus not dependent on gene expression) L1HS subfamily, has a well-established impact on senescence-related in ammation [6,7].…”
Section: Resultsmentioning
confidence: 99%
“…Garcia et al, 2016; Sisson et al, 2010) or enhanced susceptibility to intra-tracheally administered bleomycin (Barkauskas et al, 2013). More recently, senescence induction via conditional deletion of Sin3a in adult mouse AEC2s resulted in progressive pulmonary fibrosis (Yao et al, 2020). Therefore, our results are in agreement with the growing body of literature suggesting that dysfunctional AEC2s could initiate the fibrotic cascade.…”
Section: Discussionmentioning
confidence: 99%