4.5 Review

Metabolic reprogramming in the pathogenesis of chronic lung diseases, including BPD, COPD, and pulmonary fibrosis

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

  1. National Institute of General Medical Sciences of the National Institutes of Health [P20GM103652]
  2. National Natural Science Foundation of China [81472984, 81001245]
  3. Shanxi Medical University [01201301]
  4. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P20GM103652] Funding Source: NIH RePORTER

向作者/读者索取更多资源

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.

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