ArticlePloS one2013
Deficiency of ataxia telangiectasia mutated kinase modulates cardiac remodeling following myocardial infarction: involvement in fibrosis and apoptosis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- The Yin and Yang of cellular senescence in ischemia-induced myocardial injury.Trends in cardiovascular medicine · 2026Review
- The Roles of Exosome-Derived microRNAs in Cardiac Fibrosis.Molecules (Basel, Switzerland) · 2024Review
- Effects of gas signaling molecule SOThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- p53 Regulates the Extent of Fibroblast Proliferation and Fibrosis in Left Ventricle Pressure Overload.Circulation research · 2023Article
- DNA damage response signaling: A common link between cancer and cardiovascular diseases.Cancer medicine · 2023Review
- Resistin deletion protects against heart failure injury by targeting DNA damage response.Cardiovascular research · 2022Article
- Heart failure and diabetes: role of ATM.Current opinion in pharmacology · 2020Review
- Proximal tubule ATR regulates DNA repair to prevent maladaptive renal injury responses.The Journal of clinical investigation · 2019Article
- PMInternational journal of biological sciences · 2019Article
- Ataxia telangiectasia mutated kinase deficiency impairs the autophagic response early during myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2018Article
- Ataxia telangiectasia mutated kinase is an autophagic balancer at the onset of heart failure.American journal of physiology. Heart and circulatory physiology · 2018Article
- Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction.Chinese journal of integrative medicine · 2017Article
- Haplodeficiency of Ataxia Telangiectasia Mutated Accelerates Heart Failure After Myocardial Infarction.Journal of the American Heart Association · 2017Article
- DNA single-strand break-induced DNA damage response causes heart failure.Nature communications · 2017Article
- Ataxia-Telangiectasia Mutated Kinase: Role in Myocardial Remodeling.Journal of rare diseases research & treatment · 2017Article
- Article
- Ataxia telangiectasia-mutated kinase deficiency exacerbates left ventricular dysfunction and remodeling late after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2016Article
- Regulation and involvement of matrix metalloproteinases in vascular diseases.Frontiers in bioscience (Landmark edition) · 2016Review
- Attenuation of ER stress prevents post-infarction-induced cardiac rupture and remodeling by modulating both cardiac apoptosis and fibrosis.Chemico-biological interactions · 2015Article
- Ataxia-telangiectasia mutated kinase: a potential new target for suppressing inflammation in heart failure?Journal of the American Heart Association · 2014Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledAtaxia telangiectasia mutated kinase (ATM) is a cell cycle checkpoint protein activated in response to DNA damage. We recently reported that ATM plays a protective role in myocardial remodeling following β-adrenergic receptor stimulation. Here we investigated the role of ATM in cardiac remodeling using myocardial infarction (MI) as a model. METHODS AND
resultsLeft ventricular (LV) structure, function, apoptosis, fibrosis, and protein levels of apoptosis- and fibrosis-related proteins were examined in wild-type (WT) and ATM heterozygous knockout (hKO) mice 7 days post-MI. Infarct sizes were similar in both MI groups. However, infarct thickness was higher in hKO-MI group. Two dimensional M-mode echocardiography revealed decreased percent fractional shortening (%FS) and ejection fraction (EF) in both MI groups when compared to their respective sham groups. However, the decrease in %FS and EF was significantly greater in WT-MI vs hKO-MI. LV end systolic and diastolic diameters were greater in WT-MI vs hKO-MI. Fibrosis, apoptosis, and α-smooth muscle actin staining was significantly higher in hKO-MI vs WT-MI. MMP-2 protein levels and activity were increased to a similar extent in the infarct regions of both groups. MMP-9 protein levels were increased in the non-infarct region of WT-MI vs WT-sham. MMP-9 protein levels and activity were significantly lower in the infarct region of WT vs hKO. TIMP-2 protein levels similarly increased in both MI groups, whereas TIMP-4 protein levels were significantly lower in the infarct region of hKO group. Phosphorylation of p53 protein was higher, while protein levels of manganese superoxide dismutase were significantly lower in the infarct region of hKO vs WT. In vitro, inhibition of ATM using KU-55933 increased oxidative stress and apoptosis in cardiac myocytes.
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