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實驗室名稱:李宏謨老師研究室

主持人:李宏謨老師

  1. Our laboratory has been working on the molecular mechanisms of diabetic complications for many years.  We have found that advanced glycosylation end products (AGEs) may mediate inflammatory effects through NFkB, p38MAPK, and PKC dependent pathways (Lin et al., 2001; Wu et al.,2002; Wu et al., 2003).  We have raised antibodies against AGEs and developed an automatic assay for serum AGEs (Lin et al., 2002).  We demonstrated that rosiglitazone, a PPAR-g activator, has had beneficial effects on AGE-induced inflammatory responses.  These results were published in Kidney International (Chang et al., 2004; Impact factor 8.563, Ranking 4/78).  Recently, we demonstrated that a specific AGE (Nε-carboxymethyl lysine) induces mitochondrial fission and mitophagy and resulting in decreased insulin secretion from beta cells (Lo et al.,Am J Physiol endocrinol & metabolism 2015).
  2. Our other research interests are cancer research, focusing on carbohydrate metabolism in cancer cells. We found that rosiglitazone and dexamethasone may exert anti-invasive effect through induction of MAPK phoshatase-1 (MKP-1) in human glioma cells.  These results were published in Cancer Letter (Jan et al., 2008) (Impact factor 5.621, Ranking 24/211). We also showed that osteopontin may play an important role in regulating MMP-2 secretion, EMT and tumor invasion (Impact factor 6.776, Ranking 13/192).  We established that Nodal plays a causal role in the tumorigenesis of malignant gliomas (Lee et al., Oncogene, 2010;29, 3110–3123) (Impact factor 8.459, Ranking 13/211). We further demonstrated that Nodal regulates glucose and energy metabolism through HIF-1a in malignant gliomas (Lai et al., Neurooncol; 2013) (Impact factor 6.776, Ranking 13/192).  We showed that HIF-1 a regulates the shift of energy metabolism by promoting the expression of glucose transporters, glycolytic enzymes, and pyruvate dehydrogenase kinase (PDK)–1. PDK-1 represses the flux of pyruvate into acetyl-CoA, diverting carbon away from mitochondria and suppressing O2 consumption. We showed that fenofibrate lowers lipid accumulation in myotubes by modulating PPARα/AMPK/FoxO1/ATGL pathway (Chen et al., Biochem Pharmacol; 2012) (Impact factor 5.01 ranking 23/255).  We found that a-lipoic acid regulates lipid metabolism through induction of SIRT1 and activation of AMPK (Chen et al., 2012;  Diabetologia) (Impact factor 6.671, Ranking 13/128) and Kuo et al., 2012; (Eur. J. Pharmacol). Recently, we demonstrated that pyrroloquinoline quinone may resist denervation-induced skeletal muscle atrophy through activating PGC-1a and integrating mitochondrial electron transfer chain complexes (PLoS One, in press).
  3.  The principal investigator of this project has been active in international arena of academia.  He has presented his works in many international meetings.  He served as Ad Hoc reviewers for more than fifteen SCI journals.  He helped organizing the 2nd annual meeting for Asian Society of Mitochondrial Research and Medicine (ASMRM) and served as the Secretary General of that meeting in 2004.  The selected papers of this meeting were published in the Annals New York Academy of Sciences, and he was one of the two associated editors in that volume.  He was one of the major sponsors for the 6th annual meeting of ASMRM, which was held on Oct 31- Nov.2, 2009. He will chair a session and sponsor the 11th annual meeting of ASMRM, which was held on Nov.14- Nov.16, 2014 in Taipei.  He has been an active council member in both Taiwanese Society of Mitochondrial Research and Medicine (TSMRM) and Taiwanese Society of Molecular Medicine (TMM), and was the Secretary General of ASMRM from 2009-2011, and was elected as the vice president for ASMRM from 2012-2013.
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