ArticlePloS one2015
Conditional Knockout of Telomerase Reverse Transcriptase in Mesenchymal Cells Impairs Mouse Pulmonary Fibrosis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
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
22 citing papers in PubMed, 28 citations in OpenAlex.
- Telomerase Knockout in Myeloid Cells Predisposes Mice to Foam Cell Formation, Dyslipidemia, Lung Fibrosis, and Cardiac Dysfunction.Aging cell · 2026Article
- Intracellular complement Factor H promotes tumor progression through modulation of cell cycle and actin cytoskeleton.Communications biology · 2026Article
- Non-Canonical Wnt11 Signaling Regulates Pulmonary Fibrosis via Fibroblast and Alveolar Epithelial Type II Cell Crosstalk.International journal of molecular sciences · 2025Article
- Article
- Endothelial-specific telomerase inactivation causes telomere-independent cell senescence and multi-organ dysfunction characteristic of aging.Aging cell · 2024Article
- An Understanding of Mechanism-Based Approaches for 1,3,4-Oxadiazole Scaffolds as Cytotoxic Agents and Enzyme Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Research Progress in the Molecular Mechanisms, Therapeutic Targets, and Drug Development of Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- B7H3-dependent myeloid-derived suppressor cell recruitment and activation in pulmonary fibrosis.Frontiers in immunology · 2022Article
- PGC1α Regulates the Endothelial Response to Fluid Shear Stress via Telomerase Reverse Transcriptase Control of Heme Oxygenase-1.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Telomere Attrition and Clonal Hematopoiesis of Indeterminate Potential in Cardiovascular Disease.International journal of molecular sciences · 2021Review
- The dual distinct role of telomerase in repression of senescence and myofibroblast differentiation.Aging · 2021Article
- Age-associated telomere attrition in adipocyte progenitors predisposes to metabolic disease.Nature metabolism · 2020Article
- Decrypting the crosstalk of noncoding RNAs in the progression of IPF.Molecular biology reports · 2020Review
- Telomeres as Therapeutic Targets in Heart Disease.JACC. Basic to translational science · 2019Review
- Role of B7H3/IL-33 Signaling in Pulmonary Fibrosis-induced Profibrogenic Alterations in Bone Marrow.American journal of respiratory and critical care medicine · 2019Article
- The Role of Telomerase and Telomeres in Interstitial Lung Diseases: From Molecules to Clinical Implications.International journal of molecular sciences · 2019Review
- Telomerase reverse transcriptase ameliorates lung fibrosis by protecting alveolar epithelial cells against senescence.The Journal of biological chemistry · 2019Article
- Pulmonary fibrosis requires cell-autonomous mesenchymal fibroblast growth factor (FGF) signaling.The Journal of biological chemistry · 2017Article
- Twist1-induced activation of human fibroblasts promotes matrix stiffness by upregulating palladin and collagen α1(VI).Oncogene · 2016Article
- Genetic tools for identifying and manipulating fibroblasts in the mouse.Differentiation; research in biological diversity · 2016Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Telomerase is typically expressed in cellular populations capable of extended replication, such as germ cells, tumor cells, and stem cells, but is also induced in tissue injury, repair and fibrosis. Its catalytic component, telomerase reverse transcriptase (TERT) is induced in lung fibroblasts from patients with fibrotic interstitial lung disease and in rodents with bleomycin-induced pulmonary fibrosis. To evaluate the fibroblast specific role of TERT in pulmonary fibrosis, transgenic mice bearing a floxed TERT allele were generated, and then crossed with an inducible collagen α2(I)-Cre mouse line to generate fibroblast specific TERT conditional knockout mice. TERT-specific deficiency in mesenchymal cells caused attenuation of pulmonary fibrosis as manifested by reduced lung hydroxyproline content, type I collagen and α-smooth muscle actin mRNA levels. The TERT-deficient mouse lung fibroblasts displayed decreased cell proliferative capacity and higher susceptibility to induced apoptosis compared with control cells. Additionally TERT deficiency was associated with heightened α-smooth muscle actin expression indicative of myofibroblast differentiation. However the impairment of cell proliferation and increased susceptibility to apoptosis would cause a reduction in the myofibroblast progenitor population necessary to mount a successful myofibroblast-dependent fibrotic response. These findings identified a key role for TERT in fibroblast proliferation and survival essential for pulmonary fibrosis.
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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.