ReviewAging medicine (Milton (N.S.W))2020
Proinflammation, profibrosis, and arterial aging.
Review in Aging medicine (Milton (N.S.W)), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- Circulating extracellular vesicles in plasma carry accessible molecular signatures of aging in mice.bioRxiv : the preprint server for biology · 2026Article
- Engineering a Matrix-Preserving Vascular dECM Platform with Tunable Stiffness forbioRxiv : the preprint server for biology · 2026Article
- New Vistas for Withania somnifera in Signal Transduction of Inflammation and Aging.Pharmaceutical research · 2026Review
- Tanshinone I, tanshinone IIA, and cryptotanshinone: key bioactive components modulating vascular smooth muscle cell function.Frontiers in pharmacology · 2025Review
- The Role of Aging in Intracerebral Hemorrhage.Brain sciences · 2024Review
- Enhanced vasorin signaling mitigates adverse cardiovascular remodeling.Aging medicine (Milton (N.S.W)) · 2024Review
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
- Muscle quality, physical performance, and comorbidity are predicted by circulating procollagen type III N-terminal peptide (P3NP): the InCHIANTI follow-up study.GeroScience · 2024Article
- Extracellular Matrix Remodeling in Vascular Disease: Defining Its Regulators and Pathological Influence.Arteriosclerosis, thrombosis, and vascular biology · 2023Review
- Effects of Long-Term Intervention with Losartan, Aspirin and Atorvastatin on Vascular Remodeling in Juvenile Spontaneously Hypertensive Rats.Molecules (Basel, Switzerland) · 2023Article
- Increased arterial pressure volume index and cardiovascular risk score in China.BMC cardiovascular disorders · 2023Article
- Review
- Effect of Qiling Jiaogulan Powder on Pulmonary Fibrosis and Pulmonary Arteriole Remodeling in Low-Temperature-Exposed Broilers.Animals : an open access journal from MDPI · 2022Article
- Vasorin plays a critical role in vascular smooth muscle cells and arterial functions.Journal of cellular physiology · 2022Article
- Age as a risk factor in vasculitis.Seminars in immunopathology · 2022Review
- Effect of Growth Hormone Treatment on the Concentration of Selected Metabolic Markers in Girls With Turner Syndrome.Frontiers in endocrinology · 2022Article
- Single-Cell RNA-Sequencing Reveals the Cellular and Genetic Heterogeneity of Skin Scar to Verify the Therapeutic Effects and Mechanism of Action of Dispel-Scar Ointment in Hypertrophic Scar Inhibition.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Effects of puerarin on chronic inflammation: Focus on the heart, brain, and arteries.Aging medicine (Milton (N.S.W)) · 2021Review
- T cells mediate cell non-autonomous arterial ageing in mice.The Journal of physiology · 2021Article
- Age-associated proinflammatory elastic fiber remodeling in large arteries.Mechanisms of ageing and development · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a major risk factor for quintessential cardiovascular diseases, which are closely related to arterial proinflammation. The age-related alterations of the amount, distribution, and properties of the collagen fibers, such as cross-links and degradation in the arterial wall, are the major sequelae of proinflammation. In the aging arterial wall, collagen types I, II, and III are predominant, and are mainly produced by stiffened vascular smooth muscle cells (VSMCs) governed by proinflammatory signaling, leading to profibrosis. Profibrosis is regulated by an increase in the proinflammatory molecules angiotensin II, milk fat globule-EGF-VIII, and transforming growth factor-beta 1 (TGF-β1) signaling and a decrease in the vasorin signaling cascade. The release of these proinflammatory factors triggers the activation of matrix metalloproteinase type II (MMP-2) and activates profibrogenic TGF-β1 signaling, contributing to profibrosis. The age-associated increase in activated MMP-2 cleaves latent TGF-β and subsequently increases TGF-β1 activity leading to collagen deposition in the arterial wall. Furthermore, a blockade of the proinflammatory signaling pathway alleviates the fibrogenic signaling, reduces profibrosis, and prevents arterial stiffening with aging. Thus, age-associated proinflammatory-profibrosis coupling is the underlying molecular mechanism of arterial stiffening with advancing age.
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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.