ArticleHypertension (Dallas, Tex. : 1979)2008
Reduced cardiac remodeling and function in cardiac-specific EP4 receptor knockout mice with myocardial infarction.
Article in Hypertension (Dallas, Tex. : 1979), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- The Pivotal Role of Plant Derivatives and Eicosanoid Signaling Modulation in Counteracting Cardiomiopathy.International journal of molecular sciences · 2026Review
- Targeted Gene Deletion or Antagonism of the Prostaglandin E2 EP3 Receptor Protects Against Cardiac Injury Postmyocardial Infarction.Circulation. Heart failure · 2024Article
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Prostaglandin E2 affects mitochondrial function in adult mouse cardiomyocytes and hearts.Prostaglandins, leukotrienes, and essential fatty acids · 2024Article
- Control of the post-infarct immune microenvironment through biotherapeutic and biomaterial-based approaches.Drug delivery and translational research · 2023Review
- The Natriuretic Peptide System: A Single Entity, Pleiotropic Effects.International journal of molecular sciences · 2023Review
- The Link between Prostanoids and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Deleterious effects of cardiomyocyte-specific prostaglandin E2 EP3 receptor overexpression on cardiac function after myocardial infarction.Life sciences · 2023Article
- Pharmacological modulation of prostaglandin EPhysiological reports · 2022Article
- Activation of EP4 receptor limits transition of acute to chronic heart failure in lipoxygenase deficient mice.Theranostics · 2021Article
- Role of prostaglandin E2 in tissue repair and regeneration.Theranostics · 2021Review
- Atrial Natriuretic PeptideFrontiers in physiology · 2021Review
- The deleterious role of the prostaglandin EAmerican journal of physiology. Heart and circulatory physiology · 2020Article
- The cyclooxygenase-1/mPGES-1/endothelial prostaglandin EP4 receptor pathway constrains myocardial ischemia-reperfusion injury.Nature communications · 2019Article
- Article
- Prostaglandin EJournal of the American Heart Association · 2018Article
- Inflammation leads through PGE/EPEMBO molecular medicine · 2018Article
- Overexpression of prostaglandin E2 EP4 receptor improves cardiac function after myocardial infarction.Journal of molecular and cellular cardiology · 2018Article
- Prostaglandin E2 Reduces Cardiac Contractility via EP3 Receptor.Circulation. Heart failure · 2016Article
- An Update of Microsomal Prostaglandin E Synthase-1 and PGE2 Receptors in Cardiovascular Health and Diseases.Oxidative medicine and cellular longevity · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We have shown previously that cyclooxygenase-2 inhibition reduces cardiac hypertrophy and fibrosis postmyocardial infarction (MI) in a mouse model and that prostaglandin E(2) stimulates cardiomyocyte hypertrophy in vitro through its EP(4) receptor. Because the role of cardiac myocyte EP(4) in cardiac function and hypertrophy in vivo is unknown, we generated mice lacking EP(4) only in cardiomyocytes (CM- EP(4) knockout [KO]). Twelve- to 14-week-old mice were evaluated using echocardiography and histology. There were no differences in ejection fraction, myocyte cross-sectional area, and interstitial collagen fraction between KO mice and littermate controls. To test the hypothesis that EP(4) is involved in cardiac remodeling after MI, we induced MI by ligating the left anterior descending coronary artery. Two weeks later, the mice were subjected to echocardiography, and hearts were removed for histology and Western blot. There was no difference in infarct size between KO mice and controls; however, KO mice showed less myocyte cross-sectional area and interstitial collagen fraction than controls. Also, CM-EP4 KO mice had reduced ejection fraction. Because the transcription factor Stat-3 is involved in hypertrophy and protection from ischemic injury, we tested whether it was activated in control and KO mouse hearts after MI. Western blot indicated that Stat-3 was activated in control hearts after MI but not in KO hearts. Thus, CM-EP4 deletion decreased hypertrophy, fibrosis, and activation of Stat-3. However, cardiac function was unexpectedly worsened in these mice. We conclude that cardiac myocyte EP(4) plays a role in hypertrophy via activation of Stat-3, a process that seems to be cardioprotective.
Indexed as
Identifiers
What OpenQuestion holds
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.