ArticleCell2012
A thrombospondin-dependent pathway for a protective ER stress response.
Article in Cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 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
135 citing papers in PubMed, 228 citations in OpenAlex.
- Thbs1Journal of advanced research · 2026Article
- Immunomodulatory role and therapeutic potential of thrombospondin-1 during infectious diseases and autoimmunity.BMC biology · 2026Review
- Matrifibrocytes Redefine Cardiac Fibrosis: From Terminal Differentiation to Translational Modulation.Journal of cellular and molecular medicine · 2026Review
- High COMP expression promotes tumor cell proliferation and migration of rectal cancer, contributing to unfavorable prognosis and suppressive immune microenvironment.Discover oncology · 2026Article
- Circulating Biomarkers in Elderly Patients with Heart Failure: A Real-Life Study.Antioxidants (Basel, Switzerland) · 2026Article
- Descendants of hypertrophic chondrocytes promote angiogenesis by secreting THBS4 during bone growth and injury repair.Bone research · 2025Article
- Pig meniscus single-cell sequencing reveals highly active red zone chondrocyte populations involved in stemness maintenance and vascularization development.Journal of Zhejiang University. Science. B · 2025Article
- Extracellular matrix in vascular homeostasis and disease.Nature reviews. Cardiology · 2025Review
- Microrna363-5p targets thrombospondin3 to regulate pathological cardiac remodeling.Molecular and cellular biochemistry · 2025Article
- Article
- Fibroblast-specific TGF-β signaling mediates cardiac dysfunction, fibrosis, and hypertrophy in obese diabetic mice.Cardiovascular research · 2024Article
- USP20 deletion promotes eccentric cardiac remodeling in response to pressure overload and increases mortality.American journal of physiology. Heart and circulatory physiology · 2024Article
- Extracellular vesicles from human cardiac stromal cells up-regulate cardiomyocyte protective responses to hypoxia.Stem cell research & therapy · 2024Article
- Thrombospondins: Conserved mediators and modulators of metazoan extracellular matrix.International journal of experimental pathology · 2024Review
- FicD sensitizes cellular response to glucose fluctuations in mouse embryonic fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A genome-wide CRISPR/Cas9 screen identifies calreticulin as a selective repressor of ATF6α.eLife · 2024Article
- Article
- Thrombospondin 1 enhances systemic inflammation and disease severity in acute-on-chronic liver failure.BMC medicine · 2024Article
- Emerging functions of thrombospondin-1 in immunity.Seminars in cell & developmental biology · 2024Review
- Cysteine-rich with EGF-like domains 2 (CRELD2) is an endoplasmic reticulum stress-inducible angiogenic growth factor promoting ischemic heart repair.Nature cardiovascular research · 2024Article
75 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
Thrombospondin (Thbs) proteins are induced in sites of tissue damage or active remodeling. The endoplasmic reticulum (ER) stress response is also prominently induced with disease where it regulates protein production and resolution of misfolded proteins. Here we describe a function for Thbs as ER-resident effectors of an adaptive ER stress response. Thbs4 cardiac-specific transgenic mice were protected from myocardial injury, whereas Thbs4(-/-) mice were sensitized to cardiac maladaptation. Thbs induction produced a unique profile of adaptive ER stress response factors and expansion of the ER and downstream vesicles. Thbs bind the ER lumenal domain of activating transcription factor 6α (Atf6α) to promote its nuclear shuttling. Thbs4(-/-) mice showed blunted activation of Atf6α and other ER stress-response factors with injury, and Thbs4-mediated protection was lost upon Atf6α deletion. Hence, Thbs can function inside the cell during disease remodeling to augment ER function and protect through a mechanism involving regulation of Atf6α.
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What OpenQuestion holds
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.