ReviewRespiratory physiology & neurobiology2011
Alveolar macrophages initiate the systemic microvascular inflammatory response to alveolar hypoxia.
Review in Respiratory physiology & neurobiology, 2011. 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, 43 citations in OpenAlex.
- Vascular dysfunction and chronic obstructive pulmonary disease: the role of redox balance.Hypertension (Dallas, Tex. : 1979) · 2014Trial
- Lung allograft dysbiosis associates with immune response and primary graft dysfunction.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2025Article
- Distinct hypoxia-induced translational profiles of embryonic and adult-derived macrophages.iScience · 2023Article
- Article
- Bidirectional Crosstalk Between Hypoxia Inducible Factors and Glucocorticoid Signalling in Health and Disease.Frontiers in immunology · 2021Review
- Decreased Ambient Oxygen Tension Alters the Expression of Endothelin-1, iNOS and cGMP in Rat Alveolar Macrophages.International journal of medical sciences · 2019Article
- Acclimatization of the systemic microcirculation to alveolar hypoxia is mediated by an iNOS-dependent increase in nitric oxide availability.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- A Time- and Compartment-Specific Activation of Lung Macrophages in Hypoxic Pulmonary Hypertension.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- The impact of inflammation on respiratory plasticity.Experimental neurology · 2017Review
- The role of inflammation in hypoxic pulmonary hypertension: from cellular mechanisms to clinical phenotypes.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Ubiquinol decreases hemorrhagic shock/resuscitation-induced microvascular inflammation in rat mesenteric microcirculation.Physiological reports · 2014Article
- Non-Myeloid Cells are Major Contributors to Innate Immune Responses via Production of Monocyte Chemoattractant Protein-1/CCL2.Frontiers in immunology · 2014Article
- Crumbs3 is essential for proper epithelial development and viability.Molecular and cellular biology · 2014Article
- Plasma monocyte chemotactic protein-1 levels at 24 hours are a biomarker of primary graft dysfunction after lung transplantation.Translational research : the journal of laboratory and clinical medicine · 2012Article
- Simulated aeromedical evacuation does not affect systemic inflammation or organ injury in a murine model of hemorrhagic shock.Military medicine · 2012Article
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
Abstract
Alveolar hypoxia occurs as a result of a decrease in the environmental [Formula: see text] , as in altitude, or in clinical conditions associated with a global or regional decrease in alveolar ventilation. Systemic effects, in most of which an inflammatory component has been identified, frequently accompany both acute and chronic forms of alveolar hypoxia. Experimentally, it has been shown that acute exposure to environmental hypoxia causes a widespread systemic inflammatory response in rats and mice. Recent research has demonstrated that alveolar macrophages, in addition to their well known intrapulmonary functions, have systemic, extrapulmonary effects when activated, and indirect evidence suggest these cells may play a role in the systemic consequences of alveolar hypoxia. This article reviews studies showing that the systemic inflammation of acute alveolar hypoxia observed in rats is not initiated by the low systemic tissue [Formula: see text] , but rather by a chemokine, Monocyte Chemoattractant Protein-1 (MCP-1, or CCL2) released by alveolar macrophages stimulated by hypoxia and transported by the circulation. Circulating MCP-1, in turn, activates perivascular mast cells to initiate the microvascular inflammatory cascade. The research reviewed here highlights the extrapulmonary effects of alveolar macrophages and provides a possible mechanism for some of the systemic effects of alveolar hypoxia.
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.