Copyright: ©Author(s) 2026.
World J Gastrointest Oncol. Apr 15, 2026; 18(4): 117815
Published online Apr 15, 2026. doi: 10.4251/wjgo.v18.i4.117815
Published online Apr 15, 2026. doi: 10.4251/wjgo.v18.i4.117815
Figure 1 Crosstalk between mitophagy and glycolytic reprogramming mediated by the hypoxia-inducible factor 1-alpha/BCL2/adenovirus E1B 19 kDa interacting protein 3 signaling pathway.
AKT: Protein kinase B; ATP: Adenosine triphosphate; BNIP3: BCL2/adenovirus E1B 19 kDa interacting protein 3; GLUT: Glucose transporter; HK2: Hexokinase 2; HIF-1α: Hypoxia-inducible factor 1-alpha; HRE: Hypoxia responsive element; LC3: Light chain 3; LDH: Lactate dehydrogenase; MAPK: Mitogen-activated protein kinase; MMP: Matrix metalloprotease; mTOR: Mechanistic target of rapamycin; P62/SQSTM1: Sequestosome 1; OXPHOS: Oxidative phosphorylation; PFK: Phosphofructokinase; PI3K: Phosphatidylinositol 3-kinase; PKM2: Pyruvate kinase muscle isozyme M2.
- Citation: Zhang XF, Lv GH, An SJ, Yang XR, Guo WZ, Yu CY, Zhu CH. Dysregulation of the HIF-1α/BNIP3 axis links defective mitophagy to glycolytic reprogramming in a rat model of gastric precancerogenesis. World J Gastrointest Oncol 2026; 18(4): 117815
- URL: https://www.wjgnet.com/1948-5204/full/v18/i4/117815.htm
- DOI: https://dx.doi.org/10.4251/wjgo.v18.i4.117815