ArticleScience translational medicine2017
Targeted apoptosis of myofibroblasts with the BH3 mimetic ABT-263 reverses established fibrosis.
Article in Science translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
154 citing papers in PubMed, 224 citations in OpenAlex.
- Potential targets and mechanisms of Di(2-ethylhexyl) phthalate exposure in inducing chronic kidney disease: a multimodal study integrating epidemiology, network toxicology, and Mendelian randomization.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bcl-2-Dependent Persistence of Mononuclear Phagocytes Promotes Ocular Fibrosis.International journal of molecular sciences · 2026Article
- Nintedanib increases BCL-2 in fibrotic fibroblasts, enhancing ABT-199 apoptosis and fibrosis resolution.American journal of respiratory cell and molecular biology · 2026Article
- Next-generation programmable cell therapies for precision medicine.Nature reviews. Genetics · 2026Review
- Pathological Mechanism-Inspired Biomimetic Nano-Senotherapy for Reversing Experimental Atherosclerosis in ApoEAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Beyond slowing decline: leveraging apoptotic synergy to reverse pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2026Article
- Mathematical Modeling of Systemic Sclerosis and Its Treatment.Bulletin of mathematical biology · 2026Article
- Cellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers.MedComm · 2026Review
- Cell migration inducing protein alleviates adverse cardiac remodelling after ischaemia and reperfusion injury by controlling fibroblast activation.Cardiovascular research · 2026Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Fibroblasts as regulators of lung immunity, repair and fibrosis.Nature reviews. Immunology · 2026Review
- Article
- Defective branched-chain amino acid catabolism promotes pulmonary fibrosis by inducing apoptosis resistance of myofibroblasts in mice.Cell communication and signaling : CCS · 2026Article
- Fibrosis suppressive effect and mechanism of CaSR positive allosteric modulators/p-dioxanone copolymers.Drug delivery and translational research · 2026Article
- Targeting the DNA damage repair protein RAD51 alters fibroblast metabolism and enhances apoptosis in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Disulfiram attenuates immobilization-induced knee joint contracture by suppressing Caspase-1/GSDMD-mediated pyroptosis.Scientific reports · 2026Article
- Pathological Interplay of ROS With Myofibroblasts: An Impediment to Corneal Restitution.Oxidative medicine and cellular longevity · 2026Review
- Collagen in Fibrotic Diseases.Sub-cellular biochemistry · 2026Review
- Molecular insights of a Unani formulation in targeting fibrosis-associated diseases.Frontiers in pharmacology · 2026Review
- Provoking myofibroblast death: Strategies to resolve fibrosis and remodel tumor microenvironment.World journal of clinical oncology · 2025Review
94 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 6 institutions in 4 countries.
Funding
Abstract
Persistent myofibroblast activation distinguishes pathological fibrosis from physiological wound healing, suggesting that therapies selectively inducing myofibroblast apoptosis could prevent progression and potentially reverse established fibrosis in diseases such as scleroderma, a heterogeneous autoimmune disease characterized by multiorgan fibrosis. We demonstrate that fibroblast-to-myofibroblast differentiation driven by matrix stiffness increases the mitochondrial priming (proximity to the apoptotic threshold) of these activated cells. Mitochondria in activated myofibroblasts, but not quiescent fibroblasts, are primed by death signals such as the proapoptotic BH3-only protein BIM, which creates a requirement for tonic expression of the antiapoptotic protein BCL-X
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.