Zhuo Lu's research while affiliated with First Affiliated Hospital of China Medical University and other places

... These morphological changes are not merely a consequence of liver injury but actively contribute to the progression of ALD. Mitochondria are also involved in the regulation of apoptosis, and alcohol-induced mitochondrial dysfunction can trigger apoptotic pathways in hepatocytes [23,24]. This process is mediated through the release of pro-apoptotic factors like cytochrome c, further contributing to liver injury. ...

... According to the fndings, the binding of chrysophanol-8-0-glucoside (pulmatin) to the MAPK3 catalytic domain Chrysophanol, an anthraquinone metabolite obtained from the Rheum genus, has been found to possess anticancer properties in recent studies [51][52][53]. In addition, it exhibits anti-infammatory activity [54] and provides neuroprotection efects [55]. ...

... Tripartite motif containing 15 (TRIM15) enhances degradation of KEAP1 via K48-linked ubiquitination, which is the principal regulator of NRF2 degradation, causing NRF2 to escape from KEAP1-mediated degradation, and thus promoting antioxidant response, cell proliferation and invasion in NSCLC [77]. Tripartite motif containing 21 (TRIM21) can interact with GAC, leading to K63-linked ubiquitination and downregulation of protein activity, thus inhibiting proliferation and tumorigenesis in NSCLC cells [78]. Also, TRIM21 polyubiquitinates and induces proteasomal degradation of phosphofructokinase platelet (PFKP), which can be inhibited by AKT-mediated phosphorylation and F-action bundling and stress-fibre formation spatial sequestration, causing the downregulation of glycolysis in NSCLC cells [64]. ...

... Our results show that the catabolism of ketone bodies is also increased which indicates a futile circle establishment. The upregulation of the OXCT1 enzyme has been described as involved in inflammation through nuclear factor kappa B (NF-κB) activation, however, the exact signaling mechanism is not clearly known [36]. The compound downregulated OXCT1 in 5.5-fold. ...

... Toton et al. [65] recently observed PKC's influence on the autophagy of glioblastoma cells and found that a loss of PKC led to a downregulation in the expression of autophagic signals, thus presenting a potential therapeutic effect for glioblastoma. Additional studies elucidated that the Fas apoptotic inhibitory molecule regulates macroautophagy through the modulation of the mTOR pathway and PKCmediated phosphorylation in lung adenocarcinoma [66]. In hypoxic conditions, PKC interacts with protein tyrosine phosphatases-PTPN12 and triggers endothelial autophagy via AMPK activation to foster angiogenesis [67]. ...

... As the longest isoform, GNIP1 promotes the degradation of 14-3-3ζ (also called tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta (YWHAZ) through K48-linked ubiquitination. Based on that, GNIP1 can promote autophagy, proliferation and migration in NSCLC cells [69,70]. Tripartite motif containing 11 (TRIM11) ubiquitinates dual-specificity phosphatase 6 (DUSP6), subsequently promotes proliferation, and inhibits apoptosis in NSCLC cells by regulating DUSP6-ERK1/2 pathway [71]. ...