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Na Xie

Researcher at Sichuan University

Publications -  81
Citations -  5240

Na Xie is an academic researcher from Sichuan University. The author has contributed to research in topics: Lung & Pulmonary fibrosis. The author has an hindex of 36, co-authored 75 publications receiving 3618 citations. Previous affiliations of Na Xie include University of Alabama at Birmingham & Chinese Ministry of Education.

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Glycolytic Reprogramming in Myofibroblast Differentiation and Lung Fibrosis

TL;DR: The data support the novel concept of glycolytic reprogramming in the pathogenesis of lung fibrosis and provide proof-of-concept that targeting this pathway may be efficacious in treating fibrotic disorders, such as idiopathic pulmonary fibrosis.
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NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential.

TL;DR: Recent advances in the understanding of the molecular mechanisms of NAD -regulated physiological responses to stresses, the contribution of NAD + deficiency to various diseases via manipulating cellular communication networks and the potential new avenues for therapeutic intervention are summarized.
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Overcoming cancer therapeutic bottleneck by drug repurposing

TL;DR: This review presents various promising repurposed non-oncology drugs for clinical cancer management and classify these candidates into their proposed administration for either mono- or drug combination therapy.
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MicroRNA let-7c Regulates Macrophage Polarization

TL;DR: Let-7c regulates bactericidal and phagocytic activities of macrophages, two functional phenotypes implicated in macrophage polarization and targets C/EBP-δ, a transcriptional factor that plays an important role in inflammatory response.
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Pyruvate Dehydrogenase Kinase 1 Participates in Macrophage Polarization via Regulating Glucose Metabolism

TL;DR: It is found that pyruvate dehydrogenase kinase 1 (PDK1), a key regulatory enzyme in glucose metabolism, plays an important role in the differential activation of macrophages and mitochondrial respiration is enhanced during and required by the early activation of M2 macrophage.