Feng Liu

ORCID: 0000-0002-5098-1711
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About
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Research Areas
  • Adipokines, Inflammation, and Metabolic Diseases
  • Adipose Tissue and Metabolism
  • Metabolism, Diabetes, and Cancer
  • Pancreatic function and diabetes
  • interferon and immune responses
  • Protein Kinase Regulation and GTPase Signaling
  • Regulation of Appetite and Obesity
  • Diabetes and associated disorders
  • Cytokine Signaling Pathways and Interactions
  • Endoplasmic Reticulum Stress and Disease
  • PI3K/AKT/mTOR signaling in cancer
  • Gout, Hyperuricemia, Uric Acid
  • Immune cells in cancer
  • Alcohol Consumption and Health Effects
  • Renal Diseases and Glomerulopathies
  • Liver Disease Diagnosis and Treatment
  • Immune Cell Function and Interaction
  • MicroRNA in disease regulation
  • FOXO transcription factor regulation
  • Chronic Kidney Disease and Diabetes
  • Ubiquitin and proteasome pathways
  • Inflammasome and immune disorders
  • Mast cells and histamine
  • Organ Transplantation Techniques and Outcomes
  • Case Reports on Hematomas

Second Xiangya Hospital of Central South University
2016-2025

Central South University
2016-2025

Yangtze University
2025

Buchang Pharma (China)
2023-2024

Shandong University
2014-2023

Shanghai East Hospital
2022-2023

Shaanxi Institute of International Trade & Commerce
2023

Union Hospital
2018-2023

Huazhong University of Science and Technology
2023

Shanghai Public Health Clinical Center
2021-2022

Insulin resistance, a hallmark of type 2 diabetes, is associated with oxidative stress. However, the role reactive oxygen species or specific antioxidant enzymes in its development has not been tested under physiological conditions. The objective our study was to investigate impact overexpression glutathione peroxidase 1 (GPX1), an intracellular selenoprotein that reduces hydrogen peroxide (H O ) vivo , on glucose metabolism and insulin function. GPX1-overexpressing (OE) WT male mice ( n =...

10.1073/pnas.0308096101 article EN Proceedings of the National Academy of Sciences 2004-06-07

Significance Activation of the cGAMP-cGAS-STING pathway has recently been shown to mediate virus- or bacteria-induced activation innate immune response. Here we report that this also plays an important role in obesity-induced inflammation and metabolic dysfunction, beyond its well-characterized roles surveillance. We have identified adipose disulfide-bond A oxidoreductase-like protein as a key regulator mitochondrial integrity function, which protects mice from insulin resistance by...

10.1073/pnas.1708744114 article EN Proceedings of the National Academy of Sciences 2017-10-30

It has been appreciated for many years that there is a strong association between metabolism and immunity in advanced metazoan organisms. Distinct immune signatures signaling pathways have found not only but also metabolic cells. The newly discovered DNA-sensing cGAS-cGAMP-STING pathway mediates type I interferon inflammatory responses cells to defend against viral bacterial infections. Recent studies show this activated by host DNA aberrantly localized the cytosol, contributing increased...

10.2337/dbi18-0052 article EN Diabetes 2019-05-13

Adiponectin functions as an insulin sensitizer, and yet the underlying molecular mechanism(s) remains largely unknown. We found that treating C2C12 myotubes with adiponectin or rapamycin enhanced ability of to stimulate IRS-1 tyrosine phosphorylation Akt phosphorylation, concurrently reduced p70 S6 kinase at Thr389 well Ser302 Ser636/639. Overexpression dominant-negative AMP (AMPK), but not p38 MAPK, insulin-sensitizing effect adiponectin. Rapamycin, adiponectin, insulin-stimulated in HeLa...

10.1074/jbc.m700098200 article EN cc-by Journal of Biological Chemistry 2007-01-24

The binding of the adaptor protein APPL1 to adiponectin receptors is necessary for adiponectin-induced AMP-activated kinase (AMPK) activation in muscle, yet underlying molecular mechanism remains unknown. Here we show that muscle cells and metformin induce AMPK by promoting APPL1-dependent LKB1 cytosolic translocation. mediates signaling directly interacting with enhances localization anchoring this cytosol. Adiponectin also activates another upstream Ca2+/calmodulin-dependent activating...

10.1074/jbc.m109.028357 article EN cc-by Journal of Biological Chemistry 2009-06-12

Impairments in adiponectin multimerization lead to defects secretion and function are associated with diabetes, yet the underlying mechanisms remain largely unknown. We have identified an adiponectin-interacting protein, previously named GST-kappa, by yeast 2-hybrid screening. The protein contains 2 thioredoxin domains has very little sequence similarity other GST isoforms. However, this shares high secondary structure homology bacterial disulfide-bond A oxidoreductase (DsbA) is thus renamed...

10.1073/pnas.0806341105 article EN Proceedings of the National Academy of Sciences 2008-11-15

Depression is a debilitating mental illness and often comorbid with metabolic disorders such as type 2 diabetes. Adiponectin an adipocyte–derived hormone antidiabetic insulin-sensitizing properties. Here we show that adiponectin levels in plasma are reduced chronic social-defeat stress model of depression, which correlates decreased social interaction time. A reduction caused by haploinsufficiency results increased susceptibility to aversion, “anhedonia,” learned helplessness causes impaired...

10.1073/pnas.1202835109 article EN Proceedings of the National Academy of Sciences 2012-07-09

Binding of insulin receptor substrate proteins 1 and 2 (IRS1/2) to the (IR) is essential for regulation sensitivity energy homeostasis. However, mechanism IRS1/2 recruitment IR remains elusive. Here, we identify adaptor protein APPL1 as a critical molecule that promotes IRS1/2-IR interaction. forms complex with under basal conditions, this then recruited in response or adiponectin stimulation. The interaction between depends on insulin- adiponectin-stimulated phosphorylation, which greatly...

10.1016/j.celrep.2014.04.006 article EN cc-by-nc-nd Cell Reports 2014-05-01

Members of the microRNA (miR)-30 family have been reported to promote adipogenesis and inhibit osteogenesis, yet their role in regulation thermogenesis remains unknown. In this study, we show that miR-30b/c concentrations are greatly increased during adipocyte differentiation stimulated by cold exposure or β-adrenergic receptor activator. Overexpression knockdown miR-30b -30c induced suppressed, respectively, expression thermogenic genes such as UCP1 Cidea brown adipocytes. Forced also...

10.2337/db14-1117 article EN Diabetes 2015-01-09

Long-term glucocorticoid (GC) treatment induces central fat accumulation and metabolic dysfunction. We demonstrate that microRNA-27b (miR-27b) plays a role in the pathogenesis of GC-induced accumulation. Overexpression miR-27b had same effects as dexamethasone (DEX) on inhibition brown adipose differentiation energy expenditure primary adipocytes. Conversely, antagonizing function prevented DEX suppression expression tissue–specific genes. GCs transcriptionally regulate through GC...

10.2337/db14-0395 article EN Diabetes 2014-09-02

Immunogenic cell death (ICD) has been classified as a form of regulated (RCD) that is sufficient to activate an adaptive immune response. Accumulating evidence demonstrated the ability ICD reshape tumor microenvironment through emission danger signals or DAMPs, which may contribute immunotherapy. Currently, identification ICD-associated biomarkers stratify patients according their benefit from immunotherapy would be great advantage. Here, we identified two subtypes by consensus clustering....

10.3389/fimmu.2021.781466 article EN cc-by Frontiers in Immunology 2021-11-19

Alcoholic liver disease (ALD) is characterized by lipid accumulation and injury. However, how chronic alcohol consumption causes hepatic remains elusive. The present study demonstrates that activation of the mechanistic target rapamycin complex 1 (mTORC1) plays a causal role in alcoholic steatosis, inflammation, Chronic‐plus‐binge ethanol feeding led to hyperactivation mTORC1, as evidenced increased phosphorylation mTOR its downstream kinase S6 (S6K1) hepatocytes. Aberrant mTORC1 was likely...

10.1002/hep.29849 article EN Hepatology 2018-02-21

Recent studies have reported that upregulation of disulfide-bond A oxidoreductase-like protein (DsbA-L) prevented lipid-induced renal injury in diabetic nephropathy (DN). However, the role and regulation proximal tubular DsbA-L for tubulointerstitial fibrosis (TIF) remains unclear. In current study, we found a tubules-specific knockout mouse (PT-DsbA-L-KO) attenuated UUO-induced TIF, cell apoptosis inflammation. Mechanistically, interacted with Hsp90 mitochondria BUMPT cells which activated...

10.1038/s41467-020-18304-z article EN cc-by Nature Communications 2020-09-18

Obesity is a global epidemic that caused by excessive energy intake or inefficient expenditure. Brown beige fat dissipates as heat through non-shivering thermogenesis their high density of mitochondria. However, how the mitochondrial stress-induced signal coupled to cellular thermogenic program remains elusive. Here, we show DNA escape-induced activation cGAS-STING pathway negatively regulates in fat-specific DsbA-L knockout mice, model adipose tissue stress. Conversely, overexpression STING...

10.1038/s42003-020-0986-1 article EN cc-by Communications Biology 2020-05-22
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