ArticleAging and disease2011
Aging and Cardiac Fibrosis.
Article in Aging and disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 316 papers, 2 of them syntheses that pooled it.
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
316 citing papers in PubMed, 2 syntheses or guidelines pooled it, 372 citations in OpenAlex.
- Risk of dementia in patients with atrial fibrillation: Short versus long follow-up. A systematic review and meta-analysis.International journal of geriatric psychiatry · 2021Pooled it
- Pooled it
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- Mapping structural aging across human tissues reveals tissue-specific trajectories and coordinated deterioration.Nature aging · 2026Article
- Mechanics of compression-driven morphogenesis.Development (Cambridge, England) · 2026Review
- Epilepsy-induced heart damage and sudep risk: ion channelopathies, calcium homeostasis, and the therapeutic potential of resveratrol.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Emergence of heartbeat frailty in advanced age II: individual cardiovascular aging trajectories revealed by lifelong echocardiography in male mice.GeroScience · 2026Article
- Body surface potential driven personalisation of electrophysiological digital twins in hypertrophic cardiomyopathy.PLoS computational biology · 2026Article
- High Intensity Interval Training in Aged Female Mice Preserves Physical, Cognitive, and Cardiovascular Function.bioRxiv : the preprint server for biology · 2026Article
- Article
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- ML216 Alleviates Age-Related Cardiac Fibrosis by Suppressing TGF-β1 Signaling Pathway.International journal of molecular sciences · 2026Article
- Temporal AI model predicts drivers of cell state trajectories across human aging.bioRxiv : the preprint server for biology · 2026Article
- Interstitial cells and arrhythmia.American journal of physiology. Cell physiology · 2026Review
- Cardiomyocyte-derived TGFB3 attenuates cardiac fibrosis and preserves cardiac function in heart failure.Scientific reports · 2026Article
- Empagliflozin Attenuates Cardiac Fibrosis by Suppressing Fibroblast-Mediated C-C Motif Chemokine Ligand 2 Expression.Journal of the American Heart Association · 2026Article
- Anteroposterior versus anterolateral pacer pad position in patients with symptomatic bradycardia.International journal of cardiology. Heart & vasculature · 2026Article
- The Role of Thrombospondin-2 in Myocardial Fibrosis.Drug design, development and therapy · 2026Review
- Age-associated outcomes in cardiogenic shock supported with microaxial flow pumps.Annals of intensive care · 2026Article
- Clinical and Imaging Findings in 504 Cases With Left Ventricular Pseudoaneurysm Following Myocardial Infarction: A Comprehensive Systematic Review and Meta-Analysis.Cardiology research and practice · 2026Review
256 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The aging heart is characterized by morphological and structural changes that lead to its functional decline and are associated with diminished ability to meet increased demand. Extensive evidence, derived from both clinical and experimental studies suggests that the aging heart undergoes fibrotic remodeling. Age-dependent accumulation of collagen in the heart leads to progressive increase in ventricular stiffness and impaired diastolic function. Increased mechanical load, due to reduced arterial compliance, and direct senescence-associated fibrogenic actions appear to be implicated in the pathogenesis of cardiac fibrosis in the elderly. Evolving evidence suggests that activation of several distinct molecular pathways may contribute to age-related fibrotic cardiac remodeling. Reactive oxygen species, chemokine-mediated recruitment of mononuclear cells and fibroblast progenitors, transforming growth factor (TGF)-β activation, endothelin-1 and angiotensin II signaling mediate interstitial and perivascular fibrosis in the senescent heart. Reduced collagen degradation may be more important than increased de novo synthesis in the pathogenesis of aging-associated fibrosis. In contrast to the baseline activation of fibrogenic pathways in the senescent heart, aging is associated with an impaired reparative response to cardiac injury and defective activation of reparative fibroblasts in response to growth factors. Because these reparative defects result in defective scar formation, senescent hearts are prone to adverse dilative remodeling following myocardial infarction. Understanding the pathogenesis of interstitial fibrosis in the aging heart and dissecting the mechanisms responsible for age-associated healing defects following cardiac injury are critical in order to design new strategies for prevention of adverse remodeling and heart failure in elderly patients.
Identifiers
21837283PMC3153299W1515485668What 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.