Galectin-3: A Harbinger of Reactive Oxygen Species, Fibrosis, and Inflammation in Pulmonary Arterial Hypertension
| Autor: | Stephen Haigh, R. Daniel Rudic, Yusi Wang, Zsuzsanna Bordan, Feng Chen, Scott A. Barman, Keyvan Mahboubi, Xueyi Li, David Fulton |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Physiology Cardiac fibrosis Galectin 3 Clinical Biochemistry Inflammation Biochemistry 03 medical and health sciences Fibrosis medicine Animals Humans Molecular Biology General Environmental Science Pulmonary Arterial Hypertension NADPH oxidase 030102 biochemistry & molecular biology biology business.industry Cell Biology Forum Review Articles medicine.disease Pulmonary hypertension 030104 developmental biology Blood pressure medicine.anatomical_structure Galectin-3 Ventricle biology.protein Cancer research General Earth and Planetary Sciences medicine.symptom Reactive Oxygen Species business |
| Zdroj: | Antioxid Redox Signal |
| ISSN: | 1557-7716 1523-0864 |
| DOI: | 10.1089/ars.2019.7753 |
| Popis: | Significance: Pulmonary arterial hypertension (PAH) is a progressive disease arising from the narrowing of pulmonary arteries (PAs) resulting in high pulmonary arterial blood pressure and ultimately right ventricle (RV) failure. A defining characteristic of PAH is the excessive and unrelenting inward remodeling of PAs that includes increased proliferation, inflammation, and fibrosis. Critical Issues: There is no cure for PAH nor interventions that effectively arrest or reverse PA remodeling, and intensive research over the past several decades has sought to identify novel molecular mechanisms of therapeutic value. Recent Advances: Galectin-3 (Gal-3) is a carbohydrate-binding lectin remarkable for its chimeric structure, composed of an N-terminal oligomerization domain and a C-terminal carbohydrate-recognition domain. Gal-3 has been identified as a regulator of numerous changes in cell behavior that contributes to aberrant PA remodeling, including cell proliferation, inflammation, and fibrosis, but its role in PAH has remained poorly understood until recently. In contrast, pathological roles for Gal-3 have been proposed in cancer and inflammatory and fibroproliferative disorders, such as pulmonary vascular and cardiac fibrosis. Herein, we summarize the recent literature on the role of Gal-3 in the development of PAH. We provide experimental evidence supporting the ability of Gal-3 to influence reactive oxygen species production, NADPH oxidase enzyme expression, and redox signaling, which have been shown to contribute to both vascular remodeling and increased pulmonary arterial pressure. Future Directions: While several preclinical studies suggest that Gal-3 promotes hypertensive pulmonary vascular remodeling, the clinical significance of Gal-3 in human PAH remains to be established. Antioxid. Redox Signal. 00, 000–000. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|