ArticleMolecular and cellular biochemistry2001
TNF alpha is required for hypoxia-mediated right ventricular hypertrophy.
Article in Molecular and cellular biochemistry, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
- Do wearing masks and preservatives have a combined effect on skin health?Eco-Environment & Health · 2024Article
- Novel p38 Mitogen-Activated Protein Kinase Inhibitor Reverses Hypoxia-Induced Pulmonary Arterial Hypertension in Rats.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Human Mesenchymal Stem Cell Therapy Reverses Su5416/Hypoxia-Induced Pulmonary Arterial Hypertension in Mice.Frontiers in pharmacology · 2018Article
- Celecoxib prevents pressure overload-induced cardiac hypertrophy and dysfunction by inhibiting inflammation, apoptosis and oxidative stress.Journal of cellular and molecular medicine · 2016Article
- Age-dependent exacerbation of white matter stroke outcomes: a role for oxidative damage and inflammatory mediators.Stroke · 2013Article
- PKCε promotes cardiac mitochondrial and metabolic adaptation to chronic hypobaric hypoxia by GSK3β inhibition.Journal of cellular physiology · 2011Article
- Toll-like receptor 2 regulates interleukin-1beta-dependent cardiomyocyte hypertrophy triggered by Trypanosoma cruzi.Infection and immunity · 2005Article
- Counter-regulatory effects of incremental hypoxia on the transcription of a cardiac fatty acid oxidation enzyme-encoding gene.Molecular and cellular biochemistry · 2003Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia has been shown to activate the pleiotropic cytokine TNFalpha in the lung. TNFalpha in turn, is known to induce pulmonary vasoconstriction. Additional effects of this cytokine in hypoxia mediated cardiopulmonary remodeling are poorly understood. To further evaluate the role of TNFalpha in chronic hypoxia we exposed TNFalpha null (TNFalpha-/-) and wild-type mice to three weeks of hypobaric hypoxia (10% O2). Equivalent erythocytosis (Hematocrit increased by > 40%) developed in both genetic backgrounds. In contrast, right ventricular systolic pressure increased in response to three weeks of hypoxia in the wild-type mice (> or = 75%), yet was unaltered in the TNFalpha-/- mice. Concomitantly right ventricular hypertrophy was attenuated in the TNFalpha-/- mice (35 +/- 5% increase) when compared to wild-type mice (124 +/- 6% increase p < 0.001, n > or = 20). Interestingly in both strains the lung wet weights increased to a similar degree in response to hypoxia. In conclusion, our data demonstrate that TNFalpha is an integral autocoid in chronic hypoxia mediated right ventricular hypertrophy. Moreover, additional components of cardiopulmonary remodeling may be regulated by TNFalpha signaling as suggested by the negligible right ventricular systolic pressure response to hypoxia in the absence of TNFalpha.
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