Results 91 to 100 of about 13,811 (214)
Research on the Mechanism of Natural Products Acting on Chronic Obstructive Pulmonary Disease
This figure illustrates that approximately 80 natural compounds exert therapeutic effects against chronic obstructive pulmonary disease by targeting pathological mechanisms such as airway inflammation, oxidative stress, airway remodeling, mucus hypersecretion, emphysema, protease–antiprotease imbalance, apoptosis, and autophagy.
Shuna Wei, Xiaoju Liu
wiley +1 more source
p53 directly suppresses BNIP3 expression to protect against hypoxia-induced cell death
Hypoxia stabilizes the tumour suppressor p53, allowing it to function primarily as a transrepressor; however, the function of p53 during hypoxia remains unclear. In this study, we showed that p53 suppressed BNIP3 expression by directly binding to the p53-
Feng, Xi +5 more
core
Role of mitophagy in spinal cord ischemia-reperfusion injury
Spinal cord ischemia-reperfusion injury, a severe form of spinal cord damage, can lead to sensory and motor dysfunction. This injury often occurs after traumatic events, spinal cord surgeries, or thoracoabdominal aortic surgeries.
Yanni Duan +9 more
doaj +1 more source
This review illustrates the key mechanisms of osimertinib resistance in EGFR‑mutant NSCLC, including EGFR‑dependent mutations, bypass pathway activation, and SMARCA4‑mediated epigenetic regulation. We also summarize emerging targeted therapies and future perspectives to overcome EGFR‑TKI resistance.
Junfeng Guo, Qiuyuan Wen, Songqing Fan
wiley +1 more source
Blocking VDAC abolishes BNIP3-induced mitochondrial release of EndoG.
A, Mitochondria (1 mg/ml) were incubated with a recombinant GST-BNIP3 in the presence of 0.3 mg/ml of an anti-VDAC antibody or normal rabbit IgG in control. Incubation with the trunked BNIP3 (BNIP3ΔTM) was used as a control.
Jiming Kong (143823) +2 more
core +1 more source
This study maps age‐aligned cochlear and vestibular decline in SAMP8 mice, linking functional impairment with synaptic vulnerability, mitochondrial ultrastructural injury, and autophagy/mitophagy–lysosome transcriptional remodeling. The findings provide an integrated framework for understanding shared inner‐ear aging trajectories.
Jingyi Xie +14 more
wiley +1 more source
[[abstract]]The process of autophagy in heart cells maintains homeostasis during cellular stress such as hypoxia by removing aggregated proteins and damaged organelles and thereby protects the heart during the times of starvation and ischemia.
陳必誠;Chen, Bih-Cheng;Weng, Yi-Jiun;Weng, Yi-Jiun;徐布;Shibu, Marthandam Asokan;韓建國;Han, Chien-Kuo;Yueh-Sheng, C;Chen, Yueh-Sheng;She, Chia-Yao;Shen, Chia-Yao;Lin, Yueh-Min;Lin, Yueh-Min;Padma, Vijaya;Viswanadha, Vijaya Padma;Li, Hsin-Yueh;Liang, Hsin-Yueh;黃志揚;Huang, Chih-yang;*
core
C-terminal BNIP3 phosphorylation can be modulated by cellular stresses.
(A) Levels of ROS, measured by the mean fluorescence intensity of DHE. HEK 293 control cells and cells expressing WT BNIP3 for 48 hr were treated with 8-Br-cAMP for 0, 2, or 4hr immediately prior to analyzing DHE fluorescence by flow cytometry.
William A. Frazier (759144) +1 more
core +1 more source
BNIP3 induces IL6 and calcineurin/NFAT3 hypertrophic-related pathways in H9c2 cardiomyoblast cells
[[abstract]]Ischemia/reperfusion injury causes cardiomyocyte apoptosis, ventricular remodeling, leading to a dilated heart. Hypoxia is one of the causes involved in ischemia damage, and BNIP3 is a hypoxia-inducible marker and also a sensor to induce ...
黃志揚;HUANG, CHIH-YANG
core
BNIP3 is degraded by ULK1-dependent autophagy via MTORC1 and AMPK.
BNIP3 (BCL2/adenovirus E1B 19 kDa interacting protein 3) is an atypical BH3-only protein that is induced by hypoxia-inducible factor 1 (HIF1) under hypoxia. BNIP3 is primarily regulated at the transcriptional level.
Hong Gil Nam +6 more
core +2 more sources

