ReviewJournal of molecular and cellular cardiology2015
Age-associated pro-inflammatory remodeling and functional phenotype in the heart and large arteries.
Review in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 79 citations in OpenAlex.
- SIRT1: Protean roles at the nexus of health, disease, and therapeutics.Journal of cell communication and signaling · 2026Article
- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.ESC heart failure · 2025Review
- Bioinformatics approach reveals the critical role of inflammation-related genes in age-related hearing loss.Scientific reports · 2025Article
- Identification of candidate long non-coding RNAs and mRNAs associated with heart aging in mice.PeerJ · 2025Article
- Cardiac tissue-resident vesicles differentially modulate anti-fibrotic phenotype by age and sex through synergistic miRNA effects.Biomaterials · 2024Article
- The role of cardiac resident macrophage in cardiac aging.Aging cell · 2023Review
- Polarizing Macrophage Functional Phenotype to Foster Cardiac Regeneration.International journal of molecular sciences · 2023Review
- Mitochondrial Dysfunction in Cardiac Diseases and Therapeutic Strategies.Biomedicines · 2023Review
- Long-Term Impact of the Great Chinese Famine on the Risks of Specific Arrhythmias and Severe Hypertension in the Offspring at an Early Stage of Aging.Journal of personalized medicine · 2023Article
- The effect of cytokines on osteoblasts and osteoclasts in bone remodeling in osteoporosis: a review.Frontiers in immunology · 2023Review
- Inflammatory Role of Milk Fat Globule-Epidermal Growth Factor VIII in Age-Associated Arterial Remodeling.Journal of the American Heart Association · 2022Article
- Article
- The Role of Oxidative Stress in the Aging Heart.Antioxidants (Basel, Switzerland) · 2022Review
- Acute myocardial injury in patients with COVID-19: Possible mechanisms and clinical implications.World journal of clinical cases · 2022Review
- Role of circulating molecules in age-related cardiovascular and metabolic disorders.Inflammation and regeneration · 2022Review
- Cardiac alterations following experimental hip fracture - inflammaging as independent risk factor.Frontiers in immunology · 2022Article
- Effects of puerarin on chronic inflammation: Focus on the heart, brain, and arteries.Aging medicine (Milton (N.S.W)) · 2021Review
- Aged Monkeys Fed a High-Fat/High-Sugar Diet Recapitulate Metabolic Disorders and Cardiac Contractile Dysfunction.Journal of cardiovascular translational research · 2021Article
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 2 institutions in 2 countries.
Funding
Abstract
The aging population is increasing dramatically. Aging-associated stress simultaneously drives proinflammatory remodeling, involving angiotensin II and other factors, in both the heart and large arteries. The structural remodeling and functional changes that occur with aging include cardiac and vascular wall stiffening, systolic hypertension and suboptimal ventricular-arterial coupling, features that are often clinically silent and thus termed a silent syndrome. These age-related effects are the result of responses initiated by cardiovascular proinflammatory cells. Local proinflammatory signals are coupled between the heart and arteries due to common mechanical and humoral messengers within a closed circulating system. Thus, targeting proinflammatory signaling molecules would be a promising approach to improve age-associated suboptimal ventricular-arterial coupling, a major predisposing factor for the pathogenesis of clinical cardiovascular events such as heart failure.
Indexed as
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What Socratic 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 Socratic graph.