ReviewBiomolecules2025
Inflammaging and Senescence-Driven Extracellular Matrix Remodeling in Age-Associated Cardiovascular Disease.
Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- Exercise and Endothelial Function: Insights from a Redox Perspective.Current atherosclerosis reports · 2026Review
- Boron as a Context-Dependent System-Level Modulator: Mechanisms and Implications in Chronic Diseases.Biological trace element research · 2026Review
- Transcriptomic landscape of human cardiac aging: identification of cardioselective age-associated genes and predictive modeling.Biogerontology · 2026Article
- Review
- Targeting oxidative stress, senescence, and neurodegeneration: anti-aging perspectives of Urtica dioica and Centella asiatica.Inflammopharmacology · 2026Review
- Sex Differences in Mitochondrial Function: Endocrine Regulation, Immunometabolic Signaling, and Implications for Health and Disease.International journal of molecular sciences · 2026Review
- A targeted epigenetic clock for simultaneous assessment of biological aging and cancer-associated methylation drift.Clinical epigenetics · 2026Article
- Dynamics of Human Endogenous Retroviruses Expression, Proviral Load and Systemic Inflammatory Status Modulated by Physical Exercise and Aging.International journal of molecular sciences · 2026Article
- Shear-Calibrated High-Intensity Interval Training to Promote Endothelial Autophagy and Delay Vascular Senescence: A Biomarker-Guided Approach.International journal of molecular sciences · 2026Review
- Targeting the Sleep-Glymphatic-Vascular Continuum in Cerebral Small Vessel Disease: A Nutritional Perspective on Neuroprotective Potential of Tocotrienols (T3).Life (Basel, Switzerland) · 2026Review
- Network Rewiring in the Aging Immune System: From Chronic Inflammation to Age-Related Pathologies.Cells · 2026Review
- Cardio-Vascular Extracellular Matrix: The Unmet Enigma.International journal of molecular sciences · 2026Review
- Body roundness index as a predictor of 3-month readmission in elderly patients with first-episode acute heart failure.Frontiers in medicine · 2026Article
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Sirtuin 1 is a key molecular link between cellular senescence and heart failure.Frontiers in molecular medicine · 2026Review
- Unraveling the metabolic pathways between atherosclerosis and sarcopenia.Frontiers in endocrinology · 2025Review
- Metformin Attenuates Angiotensin II-Induced Cardiac Inflammaging-Like Injury Through Coordinated Nrf2 Activation and NF-κB Suppression.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular aging is a multifactorial and systemic process that contributes significantly to the global burden of cardiovascular disease, particularly in older populations. This review explores the molecular and cellular mechanisms underlying cardiovascular remodeling in age-related conditions such as hypertension, atrial fibrillation, atherosclerosis, and heart failure. Central to this process are chronic low-grade inflammation (inflammaging), oxidative stress, cellular senescence, and maladaptive extracellular matrix remodeling. These hallmarks of aging interact to impair endothelial function, promote fibrosis, and compromise cardiac and vascular integrity. Key molecular pathways-including the renin-angiotensin-aldosterone system, NF-κB, NLRP3 inflammasome, IL-6, and TGF-β signaling-contribute to the transdifferentiation of vascular cells, immune dysregulation, and progressive tissue stiffening. We also highlight the role of the senescence-associated secretory phenotype and mitochondrial dysfunction in perpetuating inflammatory and fibrotic cascades. Emerging molecular therapies offer promising strategies to reverse or halt maladaptive remodeling. These include senescence-targeting agents (senolytics), Nrf2 activators, RNA-based drugs, and ECM-modulating compounds such as MMP inhibitors. Additionally, statins and anti-inflammatory biologics (e.g., IL-1β inhibitors) exhibit pleiotropic effects that extend beyond traditional risk factor control. Understanding the molecular basis of remodeling is essential for guiding future research and improving outcomes in older adults at risk of CVD.
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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 Socratic graph.