期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 314, 期 4, 页码 1544-1554出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00521.2017
关键词
bronchopulmonary dysplasia; chronic obstructive pulmonary disease; metabolic flexibility; metabolic reprogramming; pulmonary fibrosis
资金
- National Institute of General Medical Sciences of the National Institutes of Health [P20GM103652]
- National Natural Science Foundation of China [81472984, 81001245]
- Shanxi Medical University [01201301]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P20GM103652] Funding Source: NIH RePORTER
The metabolism of nutrient substrates, including glucose, glutamine, and fatty acids, provides acetyl-CoA for the tricarboxylic acid cycle to generate energy, as well as metabolites for the biosynthesis of biomolecules, including nucleotides, proteins, and lipids. It has been shown that metabolism of glucose, fatty acid, and glutamine plays important roles in modulating cellular proliferation, differentiation, apoptosis, autophagy, senescence, and inflammatory responses. All of these cellular processes contribute to the pathogenesis of chronic lung diseases, including bronchopulmonary dysplasia, chronic obstructive pulmonary disease, and pulmonary fibrosis. Recent studies demonstrate that metabolic reprogramming occurs in patients with and animal models of chronic lung diseases, suggesting that metabolic dysregulation may participate in the pathogenesis and progression of these diseases. In this review, we briefly discuss the catabolic pathways for glucose, glutamine, and fatty acids, and focus on how metabolic reprogramming of these pathways impacts cellular functions and leads to the development of these chronic lung diseases. We also highlight how targeting metabolic pathways can be utilized in the prevention and treatment of these diseases.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据