ArticleCirculation research2010
Increasing cardiac contractility after myocardial infarction exacerbates cardiac injury and pump dysfunction.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 24 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
24 citing papers in PubMed, 47 citations in OpenAlex.
- PEDF and Its Role in Metabolic Disease, Angiogenesis, Cardiovascular Disease, and Diabetes.Biomedicines · 2025Review
- Multiscale characterization of left ventricle active behavior in the mouse.Acta biomaterialia · 2023Article
- Thymidine Phosphorylase Deficiency or Inhibition Preserves Cardiac Function in Mice With Acute Myocardial Infarction.Journal of the American Heart Association · 2023Article
- Combining three independent pathological stressors induces a heart failure with preserved ejection fraction phenotype.American journal of physiology. Heart and circulatory physiology · 2023Article
- Revealing the nanometric structural changes in myocardial infarction models by time-lapse intravital imaging.Frontiers in bioengineering and biotechnology · 2022Article
- Interaction of the Joining Region in Junctophilin-2 With the L-Type CaCirculation research · 2021Article
- Article
- Exercise training reduces ventricular arrhythmias through restoring calcium handling and sympathetic tone in myocardial infarction mice.Physiological reports · 2019Article
- Rad GTPase deletion attenuates post-ischemic cardiac dysfunction and remodeling.JACC. Basic to translational science · 2018Article
- Hyperglycemia-induced cardiac contractile dysfunction in the diabetic heart.Heart failure reviews · 2018Review
- Study of cardiovascular function using a coupled left ventricle and systemic circulation model.Journal of biomechanics · 2016Article
- Pigment Epithelium-Derived Factor (PEDF) Improves Ischemic Cardiac Functional Reserve Through Decreasing Hypoxic Cardiomyocyte Contractility Through PEDF Receptor (PEDF-R).Journal of the American Heart Association · 2016Article
- Comparative effects of urocortins and stresscopin on cardiac myocyte contractility.Journal of molecular and cellular cardiology · 2015Article
- Finding the rhythm of sudden cardiac death: new opportunities using induced pluripotent stem cell-derived cardiomyocytes.Circulation research · 2015Review
- Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarction.Circulation research · 2014Article
- Surviving the infarct: A profile of cardiac myosin binding protein-C pathogenicity, diagnostic utility, and proteomics in the ischemic myocardium.Proteomics. Clinical applications · 2014Review
- Nitroso-redox imbalance affects cardiac structure and function.Journal of the American College of Cardiology · 2013Article
- Article
- Regulation of cardiovascular cellular processes by S-nitrosylation.Biochimica et biophysica acta · 2012Review
- Therapeutic strategies based on polymeric microparticles.Journal of biomedicine & biotechnology · 2012Review
Corrections and comments
- Correction · 2020-05-07Concerns/Issues about Data · Concerns/Issues about Image · Investigation by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · Upgrade/Update of Prior Notice(s) ·
- Expression of concern · 2018-11-20Concerns/Issues about Data · Investigation by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · Updated to Correction ·
- Erratum issued
- Expression of concern
- Expression of concern
Authors and funding
19 authors at 4 institutions in 1 country.
Funding
Abstract
rationaleMyocardial infarction (MI) leads to heart failure (HF) and premature death. The respective roles of myocyte death and depressed myocyte contractility in the induction of HF after MI have not been clearly defined and are the focus of this study.
objectivesWe developed a mouse model in which we could prevent depressed myocyte contractility after MI and used it to test the idea that preventing depression of myocyte Ca(2+)-handling defects could avert post-MI cardiac pump dysfunction. METHODS AND
resultsMI was produced in mice with inducible, cardiac-specific expression of the β2a subunit of the L-type Ca(2+) channel. Myocyte and cardiac function were compared in control and β2a animals before and after MI. β2a myocytes had increased Ca(2+) current; sarcoplasmic reticulum Ca(2+) load, contraction and Ca(2+) transients (versus controls), and β2a hearts had increased performance before MI. After MI, cardiac function decreased. However, ventricular dilation, myocyte hypertrophy and death, and depressed cardiac pump function were greater in β2a versus control hearts after MI. β2a animals also had poorer survival after MI. Myocytes isolated from β2a hearts after MI did not develop depressed Ca(2+) handling, and Ca(2+) current, contractions, and Ca(2+) transients were still above control levels (before MI).
conclusionsMaintaining myocyte contractility after MI, by increasing Ca(2+) influx, depresses rather than improves cardiac pump function after MI by reducing myocyte number.
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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.