ArticleThe American journal of pathology2012
Pressure overload induces early morphological changes in the heart.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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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
53 citing papers in PubMed, 77 citations in OpenAlex.
- Proximal tubule ACE2 mediates early responses to hypertension by regulating intrarenal RAS and sodium homeostasis.JCI insight · 2026Article
- Effects of epigallocatechin-3-gallate on left ventricular remodeling and functional recovery following aortic coarctation surgery.BMC cardiovascular disorders · 2026Article
- Genetic deletion of cytoglobin exacerbates cardiac hypertrophy and inhibits cardiac fibroblast activation independent of changes in blood pressure.bioRxiv : the preprint server for biology · 2026Article
- The cardiac phospho-proteome during pressure overload in mice.Scientific data · 2025Article
- The role of mechanosignaling in the control of myocardial mass.American journal of physiology. Heart and circulatory physiology · 2025Review
- Rapid onset fibrotic remodeling and ventricular dysfunction induced by phenylephrine involve targeted reprogramming of myocyte and fibroblast transcriptomes.bioRxiv : the preprint server for biology · 2024Article
- The Extracellular Matrix and Cardiac Pressure Overload: Focus on Novel Treatment Targets.Cells · 2024Review
- Revisiting Cardiac Biology in the Era of Single Cell and Spatial Omics.Circulation research · 2024Review
- Treatment with αvβ3-integrin-specific 29P attenuates pressure-overload induced cardiac remodelling after transverse aortic constriction in mice.Journal of molecular and cellular cardiology plus · 2024Article
- Fibroblasts under pressure: cardiac fibroblast responses to hypertension and antihypertensive therapies.American journal of physiology. Heart and circulatory physiology · 2024Review
- Cardiac function in pregnant women with preeclampsia.Frontiers in cardiovascular medicine · 2024Article
- Targeting N-Myristoylation Through NMT2 Prevents Cardiac Hypertrophy and Heart Failure.JACC. Basic to translational science · 2023Article
- Aerobic Exercise Training Improves Calcium Handling and Cardiac Function in Rats with Heart Failure Resulting from Aortic Stenosis.International journal of molecular sciences · 2023Article
- Beyond cardiomyocytes: Cellular diversity in the heart's response to exercise.Journal of sport and health science · 2023Review
- Direct Reprogramming of Resident Non-Myocyte Cells and Its Potential for In Vivo Cardiac Regeneration.Cells · 2023Review
- Translational perspectives on cardiac reprogramming.Seminars in cell & developmental biology · 2022Review
- The Dysfunctional Scenario of the Major Components Responsible for Myocardial Calcium Balance in Heart Failure Induced by Aortic Stenosis.Arquivos brasileiros de cardiologia · 2022Article
- Bottom-up proteomic analysis of human adult cardiac tissue and isolated cardiomyocytes.Journal of molecular and cellular cardiology · 2022Article
- Fibroblast-specific IKK-β deficiency ameliorates angiotensin II-induced adverse cardiac remodeling in mice.JCI insight · 2021Article
- Channelling the Force to Reprogram the Matrix: Mechanosensitive Ion Channels in Cardiac Fibroblasts.Cells · 2021Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Cardiac hypertrophy, whether pathological or physiological, induces a variety of additional morphological and physiological changes in the heart, including altered contractility and hemodynamics. Events exacerbating these changes are documented during later stages of hypertrophy (usually termed pathological hypertrophy). Few studies document the morphological and physiological changes during early physiological hypertrophy. We define acute cardiac remodeling events in response to transverse aortic constriction (TAC), including temporal changes in hypertrophy, collagen deposition, capillary density, and the cell populations responsible for these changes. Cardiac hypertrophy induced by TAC in mice was detected 2 days after surgery (as measured by heart weight, myocyte width, and wall thickness) and peaked by day 7. Picrosirius staining revealed increased collagen deposition 7 days after TAC; immunostaining and flow cytometry indicated a concurrent increase in fibroblasts. The findings correlated with angiogenesis in TAC hearts; a decrease in capillary density was observed at day 2, with recovery to sham-surgery levels by day 7. Increased pericyte levels, which were observed 2 days after TAC, may mediate this angiogenic transition. Gene expression suggests a coordinated response in growth, extracellular matrix, and angiogenic factors to mediate the observed morphological changes. Our data demonstrate that morphological changes in response to cardiovascular injury occur rapidly, and the present findings allow correlation of specific events that facilitate these changes.
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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.