Lei Jiang

ORCID: 0000-0002-8596-556X
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About
Contact & Profiles
Research Areas
  • Cancer, Hypoxia, and Metabolism
  • Adipose Tissue and Metabolism
  • Mitochondrial Function and Pathology
  • Adipokines, Inflammation, and Metabolic Diseases
  • Liver Disease Diagnosis and Treatment
  • ATP Synthase and ATPases Research
  • Respiratory Support and Mechanisms
  • Cancer, Lipids, and Metabolism
  • Endoplasmic Reticulum Stress and Disease
  • Metabolism and Genetic Disorders
  • Peroxisome Proliferator-Activated Receptors
  • Metabolism, Diabetes, and Cancer
  • Sepsis Diagnosis and Treatment
  • Epigenetics and DNA Methylation
  • Intensive Care Unit Cognitive Disorders
  • Diet and metabolism studies
  • Immune cells in cancer
  • RNA modifications and cancer
  • Metabolomics and Mass Spectrometry Studies
  • Cancer Research and Treatments
  • Autophagy in Disease and Therapy
  • Plant Stress Responses and Tolerance
  • Vasculitis and related conditions
  • Lipid metabolism and biosynthesis
  • Syphilis Diagnosis and Treatment

City of Hope
2018-2025

Chinese Academy of Medical Sciences & Peking Union Medical College
2025

Peking University First Hospital
2025

Peking University
2025

Chinese Academy of Agricultural Sciences
2024-2025

Biotechnology Research Institute
2024-2025

Beckman Research Institute
2018-2025

City Of Hope National Medical Center
2019-2024

Jiangnan University
2023-2024

State Key Laboratory of Food Science and Technology
2023-2024

Mammalian cells generate citrate by decarboxylating pyruvate in the mitochondria to supply tricarboxylic acid (TCA) cycle. In contrast, hypoxia and other impairments of mitochondrial function induce an alternative pathway that produces reductively carboxylating α-ketoglutarate (AKG) via NADPH-dependent isocitrate dehydrogenase (IDH). It is unknown how reducing equivalents necessary reductive carboxylation setting impairment. Here, we identified shared metabolic features using carboxylation....

10.1016/j.celrep.2014.04.037 article EN cc-by Cell Reports 2014-05-22

Brown adipose tissue (BAT), as the main site of adaptive thermogenesis, exerts beneficial metabolic effects on obesity and insulin resistance. BAT has been previously assumed to contain a homogeneous population brown adipocytes. Utilizing multiple mouse models capable genetically labeling different cellular populations, well single-cell RNA sequencing 3D profiling, we discovered adipocyte subpopulation with low thermogenic activity coexisting classical high-thermogenic adipocytes within BAT....

10.1172/jci129167 article EN Journal of Clinical Investigation 2019-10-01

Abstract Defective arginine synthesis, due to the silencing of argininosuccinate synthase 1 (ASS1), is a common metabolic vulnerability in cancer, known as auxotrophy. Understanding how depletion kills arginine-auxotrophic cancer cells will facilitate development anti-cancer therapeutic strategies. Here we show that extracellular causes mitochondrial distress and transcriptional reprogramming. Mechanistically, starvation induces asparagine synthetase (ASNS), depleting these aspartate,...

10.1038/s42003-018-0178-4 article EN cc-by Communications Biology 2018-10-21

Inborn errors of metabolism (IEMs) link metabolic defects to human phenotypes. Modern genomics has accelerated IEM discovery, but assessing the impact genomic variants is still challenging. Here, we integrate and metabolomics identify a cause lactic acidosis epilepsy. The proband compound heterozygote for in LIPT1, which encodes lipoyltransferase required 2-ketoacid dehydrogenase (2KDH) function. Metabolomics reveals abnormalities lipids, amino acids, 2-hydroxyglutarate consistent with loss...

10.1016/j.celrep.2019.04.005 article EN cc-by-nc-nd Cell Reports 2019-04-01

Previous studies suggested that mdivi-1 (mitochondrial division inhibitor), a putative inhibitor of dynamin-related protein (DRP1), decreased cancer cell proliferation through inducing mitochondrial fusion and altering oxygen consumption. However, the metabolic reprogramming underlying DRP1 inhibition is still unclear in cells.To better understand effect inhibition, [U-13C]glucose isotope tracing was employed to assess effects several lines, DRP1-WT (wild-type) DRP1-KO (knockout) H460 lung...

10.1038/s41416-020-0778-x article EN cc-by British Journal of Cancer 2020-03-09

Abstract Background Heart rate, acidosis, consciousness, oxygenation, and respiratory rate (HACOR) have been used to predict noninvasive ventilation (NIV) failure. However, the HACOR score fails consider baseline data. Here, we aimed update take into account data test its predictive power for NIV failure primarily after 1–2 h of NIV. Methods A multicenter prospective observational study was performed in 18 hospitals China Turkey. Patients who received because hypoxemic were enrolled. In...

10.1186/s13054-022-04060-7 article EN cc-by Critical Care 2022-07-03

The endoplasmic reticulum (ER)-resident protein kinase/endoribonuclease inositol-requiring enzyme 1 (IRE1) is activated through transautophosphorylation in response to folding overload the ER lumen and maintains homeostasis by triggering a key branch of unfolded response. Here we show that mammalian IRE1α liver cells also phosphorylated kinase other than itself metabolic stimuli. Glucagon-stimulated PKA, which turn at Ser 724 , highly conserved site within activation domain. Blocking...

10.1073/pnas.1107394108 article EN Proceedings of the National Academy of Sciences 2011-09-12
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