ArticleCirculation research2011
Repair of the injured adult heart involves new myocytes potentially derived from resident cardiac stem cells.
Article in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 93 citations in OpenAlex.
- A Comprehensive Review of Dilated Cardiomyopathy in Pre-clinical Animal Models in Addition to Herbal Treatment Options and Multi-modality Imaging Strategies.Cardiovascular & hematological disorders drug targets · 2023Review
- Mechanisms and implications of sex differences in cardiac aging.The journal of cardiovascular aging · 2022Article
- Antiarrhythmic Effects of Melatonin and Omega-3 Are Linked with Protection of Myocardial Cx43 Topology and Suppression of Fibrosis in Catecholamine Stressed Normotensive and Hypertensive Rats.Antioxidants (Basel, Switzerland) · 2020Article
- Alteration in ventricular pressure stimulates cardiac repair and remodeling.Journal of molecular and cellular cardiology · 2019Article
- c-kit Haploinsufficiency impairs adult cardiac stem cell growth, myogenicity and myocardial regeneration.Cell death & disease · 2019Article
- Cardiomyocyte cell cycle dynamics and proliferation revealed through cardiac-specific transgenesis of fluorescent ubiquitinated cell cycle indicator (FUCCI).Journal of molecular and cellular cardiology · 2019Article
- Assessing Stem Cell DNA Integrity for Cardiac Cell Therapy.Journal of visualized experiments : JoVE · 2019Article
- New Myocyte Formation in the Adult Heart: Endogenous Sources and Therapeutic Implications.Circulation research · 2018Review
- Calcium-dependent potassium channels control proliferation of cardiac progenitor cells and bone marrow-derived mesenchymal stem cells.The Journal of physiology · 2018Article
- Pathologic Stimulus Determines Lineage Commitment of Cardiac C-kitCirculation · 2017Article
- Cortical Bone Stem Cell Therapy Preserves Cardiac Structure and Function After Myocardial Infarction.Circulation research · 2017Article
- miR-21 increases c-kitPeerJ · 2017Article
- Approaches to augment vascularisation and regeneration of the adult heart via the reactivated epicardium.Global cardiology science & practice · 2016Review
- TNF receptor signaling inhibits cardiomyogenic differentiation of cardiac stem cells and promotes a neuroadrenergic-like fate.American journal of physiology. Heart and circulatory physiology · 2016Article
- Acute Catecholamine Exposure Causes Reversible Myocyte Injury Without Cardiac Regeneration.Circulation research · 2016Article
- Advances in stem cell therapy for cardiovascular disease (Review).International journal of molecular medicine · 2016Review
- Mechanisms of Cardiac Regeneration.Developmental cell · 2016Review
- miR-21 Reduces Hydrogen Peroxide-Induced Apoptosis in c-kitOxidative medicine and cellular longevity · 2016Article
- Preconditioning Human Cardiac Stem Cells with an HO-1 Inducer Exerts Beneficial Effects After Cell Transplantation in the Infarcted Murine Heart.Stem cells (Dayton, Ohio) · 2015Article
- Autologous c-Kit+ Mesenchymal Stem Cell Injections Provide Superior Therapeutic Benefit as Compared to c-Kit+ Cardiac-Derived Stem Cells in a Feline Model of Isoproterenol-Induced Cardiomyopathy.Clinical and translational science · 2015Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
rationaleThe ability of the adult heart to generate new myocytes after injury is not established.
objectiveOur purpose was to determine whether the adult heart has the capacity to generate new myocytes after injury, and to gain insight into their source. METHODS AND
resultsCardiac injury was induced in the adult feline heart by infusing isoproterenol (ISO) for 10 days via minipumps, and then animals were allowed to recover for 7 or 28 days. Cardiac function was measured with echocardiography, and proliferative cells were identified by nuclear incorporation of 5-bromodeoxyuridine (BrdU; 7-day minipump infusion). BrdU was infused for 7 days before euthanasia at days 10, 17, and 38 or during injury and animals euthanized at day 38. ISO caused reduction in cardiac function with evidence of myocyte loss from necrosis. During this injury phase there was a significant increase in the number of proliferative cells in the atria and ventricle, but there was no increase in BrdU+ myocytes. cKit+ cardiac progenitor cells were BrdU labeled during injury. During the first 7 days of recovery there was a significant reduction in cellular proliferation (BrdU incorporation) but a significant increase in BrdU+ myocytes. There was modest improvement in cardiac structure and function during recovery. At day 38, overall cell proliferation was not different than control, but increased numbers of BrdU+ myocytes were found when BrdU was infused during injury.
conclusionsThese studies suggest that ISO injury activates cardiac progenitor cells that can differentiate into new myocytes during cardiac repair.
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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.