ReviewFrontiers in genetics2017
Is Vascular Amyloidosis Intertwined with Arterial Aging, Hypertension and Atherosclerosis?
Review in Frontiers in genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 18 citations in OpenAlex.
- Arterial stiffness and vascular aging: mechanisms, prevention, and therapy.Signal transduction and targeted therapy · 2025Review
- Gene Therapy Approaches for Atherosclerosis Focusing on Targeting Lipid Metabolism and Inflammation.International journal of molecular sciences · 2025Review
- Deterioration of Myocardial Global Longitudinal Strain and Its Relationship with Arterial Stiffness in Patients with Cardiac Amyloidosis: A Six-Month Follow-Up.Journal of clinical medicine · 2025Article
- The Role and Mechanism of Vascular Aging in Geriatric Vascular Diseases.Aging and disease · 2024Review
- 78 kDa Glucose-Regulated Protein Attenuates Protein Aggregation and Monocyte Adhesion Induced by Angiotensin II in Vascular Cells.International journal of molecular sciences · 2020Article
- Medin Oligomer Membrane Pore Formation: A Potential Mechanism of Vascular Dysfunction.Biophysical journal · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular amyloidosis (VA) is a component of aging, but both VA and aging move forward together. Although, not all age-related molecules are involved with VA, some molecules are involved in a crosstalk between both of them. However, the cellular mechanism by which, vascular cells are phenotypically shifted to arterial remodeling, is not only involved in aging but also linked to VA. Additionally, patients with hypertension and atherosclerosis are susceptible to VA, while amyloidosis alone may provide fertile soil for the initiation and progression of subsequent hypertension and atherosclerosis. It is known that hypertension, atherosclerosis and amyloidosis can be viewed as accelerated aging. This review summarizes the available experimental and clinical evidence to help the reader to understand the advance and underlying mechanisms for VA involvement in and interaction with aging. Taken together, it is clear that VA, hypertension and atherosclerosis are closely intertwined with arterial aging as equal partners.
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What 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.