ArticleCell death & disease2019
C1q/tumor necrosis factor-related protein-3-engineered mesenchymal stromal cells attenuate cardiac impairment in mice with myocardial infarction.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Asprosin-driven metabolic-epigenetic rewiring attenuates mesenchymal stem cell senescence with therapeutic benefits for infarcted hearts.Journal of advanced research · 2026Article
- Basement Membrane-Related Genes C1QTNF3, PTGER2, CAMK2N1, PRSS36, and B3GNT7: Novel Biomarkers for Coronary Artery Disease.Cardiovascular therapeutics · 2026Article
- Unveiling the roles of CTRP family in cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2025Review
- High-resolution analyses of the secretomes from murine C2C12 cells and primary human skeletal muscle cells reveal distinct differences in contraction-regulated myokine secretion.Frontiers in physiology · 2025Article
- The relationships between biological novel biomarkers Lp-PLAJournal of diabetes · 2024Article
- Decreased circulating CTRP3 levels in acute and chronic cardiovascular patients.Journal of molecular medicine (Berlin, Germany) · 2024Article
- The dual role of mesenchymal stem cells in apoptosis regulation.Cell death & disease · 2024Review
- P38 MAPK activated ADAM17 mediates ACE2 shedding and promotes cardiac remodeling and heart failure after myocardial infarction.Cell communication and signaling : CCS · 2023Article
- CTRP3 alleviates cardiac ischemia/reperfusion injury via LAMP1/JIP2/JNK signaling pathway.Aging · 2022Article
- The Role of Anti-Inflammatory Adipokines in Cardiometabolic Disorders: Moving beyond Adiponectin.International journal of molecular sciences · 2021Review
- Review
- Platelet extracellular vesicles enhance the proangiogenic potential of adipose-derived stem cells in vivo and in vitro.Stem cell research & therapy · 2021Article
- Mesenchymal Stem Cells Therapies on Fibrotic Heart Diseases.International journal of molecular sciences · 2021Review
- GDF11 inhibits cardiomyocyte pyroptosis and exerts cardioprotection in acute myocardial infarction mice by upregulation of transcription factor HOXA3.Cell death & disease · 2020Article
- Melatonin suppresses ER stress-dependent proapoptotic effects via AMPK in bone mesenchymal stem cells during mitochondrial oxidative damage.Stem cell research & therapy · 2020Article
- Transplantation of Umbilical Cord-Derived Mesenchymal Stem Cells Overexpressing Lipocalin 2 Ameliorates Ischemia-Induced Injury and Reduces Apoptotic Death in a Rat Acute Myocardial Infarction Model.Stem cell reviews and reports · 2020Article
- Deciphering the underlying mechanism of Xianlinggubao capsule against osteoporosis by network pharmacology.BMC complementary medicine and therapies · 2020Article
- FNDC5/irisin improves the therapeutic efficacy of bone marrow-derived mesenchymal stem cells for myocardial infarction.Stem cell research & therapy · 2020Article
- Association of CYP4F2 and CTRP9 polymorphisms and serum selenium levels with coronary artery disease.Medicine · 2020Article
- New Insights Into Implications of CTRP3 in Obesity, Metabolic Dysfunction, and Cardiovascular Diseases: Potential of Therapeutic Interventions.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesenchymal stromal cells (MSCs) transplantation offers an attractive alternative in myocardial infarctive therapy. However, poor cell engraftment and survival limit their restorative capacity. C1q/tumor necrosis factor-related protein-3 (CTRP3) inhibits reverse remodeling after myocardial infarction (MI) and was found to be secreted by MSCs in our preliminary experiments. We examined whether the overexpression of CTRP3 improved the survival of transplanted MSCs and augmented their efficacy on MI and whether silencing CTRP3 attenuated these effects. For gain-of-function analysis, MSCs overexpressing CTRP3 (LvC3-MSCs), control virus-transfected MSCs (LvNull-MSCs), MSCs alone, or phosphate-buffered saline (PBS) were injected into the peripheral areas of the infarction immediately after coronary artery ligation. For loss-of-function analysis, mice subjected to MI were randomized into groups and administered CTRP3-knockdown MSCs (LvshC3-MSCs), Lvshctrl-MSCs, MSCs, or PBS. Survival rates, cardiac function, and myocardial remodeling in mice were evaluated after 4 weeks. Injection of MSCs or LvNull-MSCs improved the left ventricular ejection fraction, inhibited cardiac fibrosis, and regulated cellular profiles of the infarction border zone 4 weeks after MI compared with those in the PBS group. Furthermore, overexpression of hCTRP3 promoted the efficacy of MSCs in the treatment of MI. However, knocking down CTRP3 impaired that. Coculture experiments confirmed that hCTRP3-enriched conditioned medium (CM) promoted MSCs migration and protected against H
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