ArticleMolecular and cellular biology2018
Defective Flux of Thrombospondin-4 through the Secretory Pathway Impairs Cardiomyocyte Membrane Stability and Causes Cardiomyopathy.
Article in Molecular and cellular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Non-telomeric function deficiency of TERT enhances pressure overload-induced mouse cardiac remodeling by activation of CNBP-mediated THBS3/ITGB1 pathway.Acta pharmacologica Sinica · 2026Article
- Descendants of hypertrophic chondrocytes promote angiogenesis by secreting THBS4 during bone growth and injury repair.Bone research · 2025Article
- Rac1 palmitoylation is required for cardiac stress adaptation and regulation of protein kinase A signaling.JCI insight · 2025Article
- Cardiomyocyte Janus kinase 1 (JAK1) signaling is required for cardiac homeostasis and cytokine-dependent activation of STAT3.Journal of molecular and cellular cardiology · 2025Article
- Rab3gap1 palmitoylation cycling modulates cardiomyocyte exocytosis and atrial natriuretic peptide release.Biophysical journal · 2025Article
- The Rab3 GTPase cycle modulates cardiomyocyte exocytosis and atrial natriuretic peptide release.Biophysical journal · 2025Article
- Effects of one-week intake of different edible oils on the urinary proteome of rats.Frontiers in nutrition · 2025Article
- Thrombospondins: Conserved mediators and modulators of metazoan extracellular matrix.International journal of experimental pathology · 2024Review
- Thrombospondin-4 deletion does not exacerbate muscular dystrophy in β-sarcoglycan-deficient and laminin α2 chain-deficient mice.Scientific reports · 2024Article
- Article
- The extracellular matrix differentially directs myoblast motility and differentiation in distinct forms of muscular dystrophy: Dystrophic matrices alter myoblast motility.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- The molecular mechanism of thrombospondin family members in cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Review
- zDHHC9 Regulates Cardiomyocyte Rab3a Activity and Atrial Natriuretic Peptide Secretion Through Palmitoylation of Rab3gap1.JACC. Basic to translational science · 2023Article
- Interleukin-33 Mediates Cardiomyopathy After Acute Kidney Injury by Signaling to Cardiomyocytes.Circulation · 2023Article
- Ankyrin-B is lipid-modified byFrontiers in physiology · 2023Article
- Colocalization of corneal resistance factor GWAS loci with GTEx e/sQTLs highlights plausible candidate causal genes for keratoconus postnatal corneal stroma weakening.Frontiers in genetics · 2023Article
- PDIA3/ERp57 promotes a matrix-rich secretome that stimulates fibroblast adhesion through CCN2.American journal of physiology. Cell physiology · 2022Article
- Quantitative proteomic analysis reveals the effects of mu opioid agonists on HT22 cells.Frontiers in pharmacology · 2022Article
- THBS4/integrin α2 axis mediates BM-MSCs to promote angiogenesis in gastric cancer associated with chronicAging · 2021Article
- Effects of thrombospondin-4 on pro-inflammatory phenotype differentiation and apoptosis in macrophages.Cell death & disease · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Thrombospondins are stress-inducible secreted glycoproteins with critical functions in tissue injury and healing. Thrombospondin-4 (Thbs4) is protective in cardiac and skeletal muscle, where it activates an adaptive endoplasmic reticulum (ER) stress response, induces expansion of the ER, and enhances sarcolemmal stability. However, it is unclear if Thbs4 has these protective functions from within the cell, from the extracellular matrix, or from the secretion process itself. In this study, we generated transgenic mice with cardiac cell-specific overexpression of a secretion-defective mutant of Thbs4 to evaluate its exclusive intracellular and secretion-dependent functions. Like wild-type Thbs4, the secretion-defective mutant upregulates the adaptive ER stress response and expands the ER and intracellular vesicles in cardiomyocytes. However, only the secretion-defective Thbs4 mutant produces cardiomyopathy with sarcolemmal weakness and rupture that is associated with reduced adhesion-forming glycoproteins in the membrane. Similarly, deletion of
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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.