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Updated: Jul 25, 2025
The Left Pneumonectomy Combined with Monocrotaline or Sugen as a Model of Pulmonary Hypertension in Rats
Published on: March 8, 2019
Metabolic Deregulation in Pulmonary Hypertension.
Rajamma Mathew1,2, Sanda Iacobas3, Jing Huang4
1Department of Pediatrics, New York Medical College, Valhalla, NY 10595, USA.
Pulmonary arterial hypertension (PAH) involves metabolic changes, including altered glucose transport and glycolysis. This study reveals significant metabolic pathway remodeling in PAH rat models, highlighting dysregulation as a key pathogenic factor.
Area of Science:
- Biochemistry
- Molecular Biology
- Pathophysiology
Background:
- Pulmonary arterial hypertension (PAH) has high morbidity and mortality, partly due to metabolic issues.
- Previous work identified specific gene increases in PAH models.
Purpose of the Study:
- To identify metabolic deregulation in PAH.
- To analyze gene expression changes in PAH rat models.
Main Methods:
- Induced PAH in rats via hypoxia or monocrotaline.
- Utilized Western blot, immunofluorescence, and transcriptomic data analysis.
- Applied the Genomic Fabric Paradigm for analysis.
Main Results:
- Identified increased Slc2a1, Ngf, and Nfe2l2 in PAH models.
- Found significant remodeling of the citrate cycle, pyruvate metabolism, and glycolysis/gluconeogenesis.
- Glycolysis/gluconeogenesis was the most affected pathway across all models.
- Observed altered fructose and mannose metabolism with Pmm1 replacing Pmm2.
- Detected regulation of genes involved in PAH channelopathies.
Conclusions:
- Metabolic dysregulation is a significant factor in PAH pathogenesis.
- Specific metabolic pathways and gene expressions are altered in PAH.
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