ArticleRespiratory research2013
Apoptosis inhibitor of macrophage (AIM) expression in alveolar macrophages in COPD.
Article in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 27 citations in OpenAlex.
- Immune-metabolic positive feedback model in COPD: cross-mechanisms and potential intervention strategies.Frontiers in cell and developmental biology · 2026Review
- Metabolic reprogramming of macrophages in chronic obstructive pulmonary disease.Frontiers in immunology · 2025Review
- The effects of apoptosis inhibitor of macrophage in kidney diseases.European journal of medical research · 2024Review
- ISM1 protects lung homeostasis via cell-surface GRP78-mediated alveolar macrophage apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Apoptosis inhibitor of macrophage as a biomarker for disease activity in Japanese children with IgA nephropathy and Henoch-Schönlein purpura nephritis.Pediatric research · 2021Article
- Epidemiologic Evidence of and Potential Mechanisms by Which Second-Hand Smoke Causes Predisposition to Latent and Active Tuberculosis.Immune network · 2018Review
- Characterisation of lung macrophage subpopulations in COPD patients and controls.Scientific reports · 2017Article
- COPD monocytes demonstrate impaired migratory ability.Respiratory research · 2017Article
- Association of apoptosis inhibitor of macrophage (AIM) expression with urinary protein and kidney dysfunction.Clinical and experimental nephrology · 2017Article
- Nitrative stress, oxidative stress and plasma endothelin levels after inhalation of particulate matter and ozone.Particle and fibre toxicology · 2015Article
- Genetic variants in ADAM33 are associated with airway inflammation and lung function in COPD.BMC pulmonary medicine · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMarked accumulation of alveolar macrophages (AM) conferred by apoptosis resistance has been implicated in pathogenesis of chronic obstructive pulmonary disease (COPD). Apoptosis inhibitor of macrophage (AIM), has been shown to be produced by mature tissue macrophages and AIM demonstrates anti-apoptotic property against multiple apoptosis-inducing stimuli. Accordingly, we attempt to determine if AIM is expressed in AM and whether AIM is involved in the regulation of apoptosis in the setting of cigarette smoke extract (CSE) exposure.
methodsImmunohistochemical evaluations of AIM were performed. Immunostaining was assessed by counting total and positively staining AM numbers in each case (n = 5 in control, n = 5 in non-COPD smoker, n = 5 in COPD). AM were isolated from bronchoalveolar lavage fluid (BALF). The changes of AIM expression levels in response to CSE exposure in AM were evaluated. Knock-down of anti-apoptotic Bcl-xL was mediated by siRNA transfection. U937 monocyte-macrophage cell line was used to explore the anti-apoptotic properties of AIM.
resultsThe numbers of AM and AIM-positive AM were significantly increased in COPD lungs. AIM expression was demonstrated at both mRNA and protein levels in isolated AM, which was enhanced in response to CSE exposure. AIM significantly increased Bcl-xL expression levels in AM and Bcl-xL was involved in a part of anti-apoptotic mechanisms of AIM in U937 cells in the setting of CSE exposure.
conclusionsThese results suggest that AIM expression in association with cigarette smoking may be involved in accumulation of AM in COPD.
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.