ArticleAmerican journal of respiratory cell and molecular biology2016
Targeting Inhibitor of Apoptosis Proteins Protects from Bleomycin-Induced Lung Fibrosis.
Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 47 citations in OpenAlex.
- Reimagining Fibrosis Research, Outcomes, and Therapeutics Through the Lens of Resolution.Seminars in respiratory and critical care medicine · 2025Review
- Inhalable Hsa-miR-30a-3p Liposomes Attenuate Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Progressive lung fibrosis: reprogramming a genetically vulnerable bronchoalveolar epithelium.The Journal of clinical investigation · 2025Review
- Genome-wide CRISPR/Cas9 screening identifies key profibrotic regulators of TGF-β1-induced epithelial-mesenchymal transformation and pulmonary fibrosis.Frontiers in molecular biosciences · 2025Article
- Discoidin domain receptor 2 signaling through PIK3C2α in fibroblasts promotes lung fibrosis.The Journal of pathology · 2024Article
- Inhibition of discoidin domain receptor 2 reveals kinase-dependent and kinase-independent functions in regulating fibroblast activity.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023Review
- Regulation of Mesenchymal Cell Fate by Transfer of Active Gasdermin-D via Monocyte-Derived Extracellular Vesicles.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Inhibition of antiapoptotic BCL-2 proteins with ABT-263 induces fibroblast apoptosis, reversing persistent pulmonary fibrosis.JCI insight · 2023Article
- A four-part guide to lung immunology: Invasion, inflammation, immunity, and intervention.Frontiers in immunology · 2023Review
- Comprehensive analysis of an endoplasmic reticulum stress-related gene prediction model and immune infiltration in idiopathic pulmonary fibrosis.Frontiers in immunology · 2023Article
- Blockade of caspase cascade overcomes malaria-associated acute respiratory distress syndrome in mice.Cell death & disease · 2022Article
- XIAP Knockdown in Alcohol-Associated Liver Disease Models Exhibits DivergentFrontiers in physiology · 2021Article
- Type I Collagen Signaling Regulates Opposing Fibrotic Pathways through αAmerican journal of respiratory cell and molecular biology · 2020Article
- Retinoic acid signalling in fibro/adipogenic progenitors robustly enhances muscle regeneration.EBioMedicine · 2020Article
- You Say You Want a Resolution (of Fibrosis).American journal of respiratory cell and molecular biology · 2020Review
- Diverse Injury Pathways Induce Alveolar Epithelial Cell CCL2/12, Which Promotes Lung Fibrosis.American journal of respiratory cell and molecular biology · 2020Article
- Transcriptomic profiling of microglia and astrocytes throughout aging.Journal of neuroinflammation · 2020Article
- Evasion of apoptosis by myofibroblasts: a hallmark of fibrotic diseases.Nature reviews. Rheumatology · 2020Review
- Urokinase Plasminogen Activator Overexpression Reverses Established Lung Fibrosis.Thrombosis and haemostasis · 2019Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Accumulation of apoptosis-resistant fibroblasts is a hallmark of pulmonary fibrosis. We hypothesized that disruption of inhibitor of apoptosis protein (IAP) family proteins would limit lung fibrosis. We first show that transforming growth factor-β1 and bleomycin increase X-linked IAP (XIAP) and cellular IAP (cIAP)-1 and -2 in murine lungs and mesenchymal cells. Functional blockade of XIAP and the cIAPs with AT-406, an orally bioavailable second mitochondria-derived activator of caspases (Smac) mimetic, abrogated bleomycin-induced lung fibrosis when given both prophylactically and therapeutically. To determine whether the reduction in fibrosis was predominantly due to AT-406-mediated inhibition of XIAP, we compared the fibrotic response of XIAP-deficient mice (XIAP(-/y)) with littermate controls and found no difference. We found no alterations in total inflammatory cells of either wild-type mice treated with AT-406 or XIAP(-/y) mice. AT-406 treatment limited CCL12 and IFN-γ production, whereas XIAP(-/y) mice exhibited increased IL-1β expression. Surprisingly, XIAP(-/y) mesenchymal cells had increased resistance to Fas-mediated apoptosis. Functional blockade of cIAPs with AT-406 restored sensitivity to Fas-mediated apoptosis in XIAP(-/y) mesenchymal cells in vitro and increased apoptosis of mesenchymal cells in vivo, indicating that the increased apoptosis resistance in XIAP(-/y) mesenchymal cells was the result of increased cIAP expression. Collectively, these results indicate that: (1) IAPs have a role in the pathogenesis of lung fibrosis; (2) a congenital deficiency of XIAP may be overcome by compensatory mechanisms of other IAPs; and (3) broad functional inhibition of IAPs may be an effective strategy for the treatment of lung fibrosis by promoting mesenchymal cell apoptosis.
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