ReviewTrends in cardiovascular medicine2011
AIP1 in graft arteriosclerosis.
Review in Trends in cardiovascular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 13 citations in OpenAlex.
- DAB2IP: unifying cardiovascular pathogenesis and cardiovascular brain crosstalk.Frontiers in cardiovascular medicine · 2026Review
- SRF SUMOylation modulates smooth muscle phenotypic switch and vascular remodeling.Nature communications · 2024Article
- ASK1-Interacting Protein 1 Acts as a Novel Predictor of Type 2 Diabetes.Frontiers in endocrinology · 2022Article
- Short AIP1 (ASK1-Interacting Protein-1) Isoform Localizes to the Mitochondria and Promotes Vascular Dysfunction.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Endothelial AIP1 Regulates Vascular Remodeling by Suppressing NADPH Oxidase-2.Frontiers in physiology · 2018Article
- Block one, unleash a hundred. Mechanisms of DAB2IP inactivation in cancer.Cell death and differentiation · 2017Review
- AIP1-mediated stress signaling in atherosclerosis and arteriosclerosis.Current atherosclerosis reports · 2015Review
- Immune mechanisms in medium and large-vessel vasculitis.Nature reviews. Rheumatology · 2013Review
- SOCS1 prevents graft arteriosclerosis by preserving endothelial cell function.Journal of the American College of CardiologyArticle
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
Graft arteriosclerosis (GA), the major cause of late cardiac allograft failure, is characterized by a diffuse, concentric arterial intimal hyperplasia composed of infiltrating host T cells, macrophages, and predominantly graft-derived smooth muscle-like cells that proliferate and elaborate extracellular matrix, resulting in luminal obstruction and allograft ischemia. Interferon-γ (IFN-γ), a proinflammatory cytokine produced by effector T cells, is a critical mediator for smooth muscle-like cell proliferation. We have exploited the power of mouse genetics to examine the function of AIP1, a signaling adaptor molecule involved in vascular inflammation, in two newly established IFN-γ-mediated models of GA. Our data suggest that AIP1 inhibits intimal formation in GA by downregulating IFN-γ-activated migratory and proliferative signaling pathways in smooth muscle-like cells.
Indexed as
Identifiers
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.