ArticlePloS one2017
Senescence as a novel mechanism involved in β-adrenergic receptor mediated cardiac hypertrophy.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Lipofuscin: Wear Pigment or Alarm Signal for Cardiac AlloGraft Vasculopathy?Diagnostics (Basel, Switzerland) · 2026Article
- Isoproterenol Induces Cardiac Injury and Senescence in Sprague-Dawley Rats: A Cost-Effective Pharmacological Model.Biomedicines · 2026Article
- FTO-dependent m6A methylation mediates gestational diabetes mellitus-induced offspring cardiac senescent hypertrophy and dysfunction.iScience · 2026Article
- Senescence-like Phenotype After Chronic Exposure to Isoproterenol in Primary Quiescent Immune Cells.Biomolecules · 2024Article
- HIV Protein Nef Induces Cardiomyopathy Through Induction of Bcl2 and p21.International journal of molecular sciences · 2024Article
- Therapeutic opportunities for senolysis in cardiovascular disease.The FEBS journal · 2023Review
- Extracellular Vesicles and Cardiac Aging.Advances in experimental medicine and biology · 2023Article
- The role of cellular senescence in cardiac disease: basic biology and clinical relevance.Nature reviews. Cardiology · 2022Review
- Metoprolol Protects Against Arginine Vasopressin-Induced Cellular Senescence in H9C2 Cardiomyocytes by Regulating the Sirt1/p53/p21 Axis.Cardiovascular toxicology · 2022Article
- Cardiac robustness regulated by reactive sulfur species.Journal of clinical biochemistry and nutrition · 2022Article
- Review
- Selective intrarenal delivery of mesenchymal stem cell-derived extracellular vesicles attenuates myocardial injury in experimental metabolic renovascular disease.Basic research in cardiology · 2020Article
- Cardiomyocyte Contractility and Autophagy in a Premature Senescence Model of Cardiac Aging.Oxidative medicine and cellular longevity · 2020Article
- Transcriptional Profiles of Skeletal Muscle Associated With Increasing Severity of White Striping in Commercial Broilers.Frontiers in physiology · 2020Article
- Sinapic Acid Promotes Browning of 3T3-L1 Adipocytes via p38 MAPK/CREB Pathway.BioMed research international · 2020Article
- Honokiol antagonizes doxorubicin‑induced cardiomyocyte senescence by inhibiting TXNIP‑mediated NLRP3 inflammasome activation.International journal of molecular medicine · 2020Article
- miR-29a attenuates cardiac hypertrophy through inhibition of PPARδ expression.Journal of cellular physiology · 2019Article
- Extracellular matrix roles in cardiorenal fibrosis: Potential therapeutic targets for CVD and CKD in the elderly.Pharmacology & therapeutics · 2019Review
- New Insights into Chronological Mobility of Retrotransposons In Vivo.Oxidative medicine and cellular longevity · 2019Article
- Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathological cardiac hypertrophy used to be elucidated by biomechanical, stretch-sensitive or neurohumoral mechanisms. However, a series of hints have indicated that hypertrophy process simulates senescence program. However, further evidence need to be pursued. To verify this hypothesis and examine whether cardiac senescence is a novel mechanism of hypertrophy induced by isoproterenol, 2-month-old male Sprague Dawley rats were subjected to isoproterenol infusion (0.25mg/kg/day) for 7 days by subcutaneous injection). Key characteristics of senescence (senescence-associated β-galactosidase activity, lipofuscin, expression of cyclin-dependent kinase inhibitors) were examined in cardiac hypertrophy model. Senescence-like phenotype, such as increased senescence-associated β-galactosidase activity, accumulation of lipofuscin and high levels of cyclin-dependent kinase inhibitors (e.g. p16, p19, p21 and p53) was found along the process of cardiac hypertrophy. Cardiac-specific transcription factor GATA4 increased in isoproterenol-treated cardiomyocytes as well. We further found that myocardial hypertrophy could be inhibited by resveratrol, an anti-aging compound, in a dose-dependent manner. Our results showed for the first time that cardiac senescence is involved in the process of pathological cardiac hypertrophy induced by isoproterenol.
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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.