ArticleThe Journal of clinical investigation1993
Neointimal macrophages colocalize with extracellular matrix gene expression in human atherosclerotic pulmonary arteries.
Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 62 citations in OpenAlex.
- Pulmonary hypertension secondary to pulmonary fibrosis: clinical data, histopathology and molecular insights.Respiratory research · 2020Review
- Molecular pathogenesis of pulmonary arterial hypertension.The Journal of clinical investigation · 2012Review
- Emergence of fibroblasts with a proinflammatory epigenetically altered phenotype in severe hypoxic pulmonary hypertension.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Identification of markers that distinguish monocyte-derived fibrocytes from monocytes, macrophages, and fibroblasts.PloS one · 2009Article
- The 'sweet' and 'bitter' involvement of glycosaminoglycans in lung diseases: pharmacotherapeutic relevance.British journal of pharmacology · 2009Review
- Molecular pathogenesis of pulmonary arterial hypertension.The Journal of clinical investigation · 2008Review
- Pulmonary hemodynamics modify the rat pulmonary artery response to injury. A neointimal model of pulmonary hypertension.The American journal of pathology · 1997Article
- Tenascin-C, proliferation and subendothelial fibronectin in progressive pulmonary vascular disease.The American journal of pathology · 1997Article
- The role of vascular injury and hemodynamics in rat pulmonary artery remodeling.The Journal of clinical investigation · 1996Article
- Dynamics of Vascular Remodeling: An Overview and Bibliography.Journal of thrombosis and thrombolysis · 1996Article
- Matrix proteins associated with bone calcification are present in human vascular smooth muscle cells grown in vitro.In vitro cellular & developmental biology. Animal · 1995Article
- Active proliferation of different cell types, including lymphocytes, in human atherosclerotic plaques.The American journal of pathology · 1995Article
- Active macrophage-associated TGF-beta co-localizes with type I procollagen gene expression in atherosclerotic human pulmonary arteries.The American journal of pathology · 1995Article
- VLA-4 and lymphocyte trafficking in immune-inflammatory states: novel therapeutic approaches in allograft arteriopathy.Springer seminars in immunopathology · 1995Review
- 92-kD gelatinase is produced by eosinophils at the site of blister formation in bullous pemphigoid and cleaves the extracellular domain of recombinant 180-kD bullous pemphigoid autoantigen.The Journal of clinical investigation · 1994Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Vascular remodeling in adult atherosclerotic pulmonary arteries is characterized by discrete areas of neointimal extracellular matrix gene expression, suggesting regulation by local factors. Though the factors responsible for inducing matrix gene expression in atherosclerotic lesions are largely unknown, several observations suggest macrophages may be a focal source of those factors. Immunohistochemistry confirmed the presence of macrophages in the neointima of atherosclerotic elastic pulmonary arteries from patients with unexplained pulmonary hypertension. Areas of neointima containing dense clusters of macrophages were separated by sparsely populated areas. Foamy macrophages resided more deeply within the neointima than nonfoamy macrophages, which were found more often subjacent to the endothelium or within the lumenal one-third of the neointima. Combined immunohistochemistry-in situ hybridization indicated neointimal fibronectin and type I procollagen gene expression was intimately associated only with nonfoamy neointimal macrophages. These observations suggest that: (a) nonfoamy neointimal macrophages participate in the local regulation of extracellular matrix gene expression in atherosclerotic pulmonary arteries; (b) foamy macrophages, which are not associated with matrix gene expression, have undergone modulation of their secretory phenotype.
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.