Dongsheng Cai

Summary

Affiliation: Albert Einstein College of Medicine
Country: USA

Publications

  1. doi request reprint Neuroinflammation in overnutrition-induced diseases
    Dongsheng Cai
    Department of Molecular Pharmacology, Institute of Aging, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, USA
    Vitam Horm 91:195-218. 2013
  2. pmc Neuroinflammation and neurodegeneration in overnutrition-induced diseases
    Dongsheng Cai
    Department of Molecular Pharmacology, Institute of Aging, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Trends Endocrinol Metab 24:40-7. 2013
  3. doi request reprint Hypothalamic inflammation: a double-edged sword to nutritional diseases
    Dongsheng Cai
    Department of Molecular Pharmacology, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Ann N Y Acad Sci 1243:E1-39. 2011
  4. pmc Treatment of obesity and diabetes using oxytocin or analogs in patients and mouse models
    Hai Zhang
    Department of Molecular Pharmacology, Diabetes Research Center, Institute of Aging, Albert Einstein College of Medicine, Bronx, New York, USA
    PLoS ONE 8:e61477. 2013
  5. pmc Hypoxia-inducible factor directs POMC gene to mediate hypothalamic glucose sensing and energy balance regulation
    Hai Zhang
    Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, United States of America
    PLoS Biol 9:e1001112. 2011
  6. pmc Hypothalamic programming of systemic ageing involving IKK-β, NF-κB and GnRH
    Guo Zhang
    Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Nature 497:211-6. 2013
  7. pmc Disruption of neurogenesis by hypothalamic inflammation in obesity or aging
    Sudarshana Purkayastha
    Department of Molecular Pharmacology, Diabetes Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY, 10461, USA
    Rev Endocr Metab Disord 14:351-6. 2013
  8. pmc IKKβ/NF-κB disrupts adult hypothalamic neural stem cells to mediate a neurodegenerative mechanism of dietary obesity and pre-diabetes
    Juxue Li
    Department of Molecular Pharmacology, Bronx, New York 10461, USA
    Nat Cell Biol 14:999-1012. 2012
  9. pmc Obesity- and aging-induced excess of central transforming growth factor-β potentiates diabetic development via an RNA stress response
    Jingqi Yan
    1 Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, USA 2 Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, USA 3 Institute of Aging, Albert Einstein College of Medicine, Bronx, New York, USA 4
    Nat Med 20:1001-8. 2014
  10. pmc Uncoupling the mechanisms of obesity and hypertension by targeting hypothalamic IKK-β and NF-κB
    Sudarshana Purkayastha
    Department of Molecular Pharmacology, Albert Einstein College of Medicine, New York, New York, USA
    Nat Med 17:883-7. 2011

Collaborators

Detail Information

Publications22

  1. doi request reprint Neuroinflammation in overnutrition-induced diseases
    Dongsheng Cai
    Department of Molecular Pharmacology, Institute of Aging, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, USA
    Vitam Horm 91:195-218. 2013
    ....
  2. pmc Neuroinflammation and neurodegeneration in overnutrition-induced diseases
    Dongsheng Cai
    Department of Molecular Pharmacology, Institute of Aging, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Trends Endocrinol Metab 24:40-7. 2013
    ..Targeting neuroinflammation and neurodegeneration will provide promising approaches for treating obesity and other overnutrition-related diseases...
  3. doi request reprint Hypothalamic inflammation: a double-edged sword to nutritional diseases
    Dongsheng Cai
    Department of Molecular Pharmacology, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Ann N Y Acad Sci 1243:E1-39. 2011
    ....
  4. pmc Treatment of obesity and diabetes using oxytocin or analogs in patients and mouse models
    Hai Zhang
    Department of Molecular Pharmacology, Diabetes Research Center, Institute of Aging, Albert Einstein College of Medicine, Bronx, New York, USA
    PLoS ONE 8:e61477. 2013
    ..In conclusion, oxytocin and its analogs have multi-level effects in improving weight control, insulin sensitivity and insulin secretion, and bear potentials for being developed as therapeutic peptides for obesity and diabetes...
  5. pmc Hypoxia-inducible factor directs POMC gene to mediate hypothalamic glucose sensing and energy balance regulation
    Hai Zhang
    Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, United States of America
    PLoS Biol 9:e1001112. 2011
    ..In conclusion, HIF controls hypothalamic POMC gene to direct the central nutrient sensing in regulation of energy and body weight balance...
  6. pmc Hypothalamic programming of systemic ageing involving IKK-β, NF-κB and GnRH
    Guo Zhang
    Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Nature 497:211-6. 2013
    ....
  7. pmc Disruption of neurogenesis by hypothalamic inflammation in obesity or aging
    Sudarshana Purkayastha
    Department of Molecular Pharmacology, Diabetes Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY, 10461, USA
    Rev Endocr Metab Disord 14:351-6. 2013
    ..This article reviews the crucial role of hypothalamic inflammation in affecting neural stem cells which mediates the neurodegenerative mechanisms of causing metabolic derangements as well as aging-associated disorders or diseases. ..
  8. pmc IKKβ/NF-κB disrupts adult hypothalamic neural stem cells to mediate a neurodegenerative mechanism of dietary obesity and pre-diabetes
    Juxue Li
    Department of Molecular Pharmacology, Bronx, New York 10461, USA
    Nat Cell Biol 14:999-1012. 2012
    ..In conclusion, adult htNSCs are important for the central regulation of metabolic physiology, and IKKβ/NF-κB-mediated impairment of adult htNSCs is a critical neurodegenerative mechanism for obesity and related diabetes...
  9. pmc Obesity- and aging-induced excess of central transforming growth factor-β potentiates diabetic development via an RNA stress response
    Jingqi Yan
    1 Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, USA 2 Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, USA 3 Institute of Aging, Albert Einstein College of Medicine, Bronx, New York, USA 4
    Nat Med 20:1001-8. 2014
    ..These results reveal an atypical, mRNA metabolism-driven hypothalamic nuclear factor-κB activation, a mechanism that links obesity as well as aging to hypothalamic inflammation and ultimately to type 2 diabetes. ..
  10. pmc Uncoupling the mechanisms of obesity and hypertension by targeting hypothalamic IKK-β and NF-κB
    Sudarshana Purkayastha
    Department of Molecular Pharmacology, Albert Einstein College of Medicine, New York, New York, USA
    Nat Med 17:883-7. 2011
    ..Breaking this pathogenic link may represent an avenue for controlling obesity-related hypertension and CVD without requiring obesity control...
  11. pmc Defective hypothalamic autophagy directs the central pathogenesis of obesity via the IkappaB kinase beta (IKKbeta)/NF-kappaB pathway
    Qingyuan Meng
    Department of Molecular Pharmacology and Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Biol Chem 286:32324-32. 2011
    ....
  12. pmc Circadian intervention of obesity development via resting-stage feeding manipulation or oxytocin treatment
    Guo Zhang
    Department of Molecular Pharmacology and Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Am J Physiol Endocrinol Metab 301:E1004-12. 2011
    ..In conclusion, resting-stage oxytocin release and feeding activity represent a critical circadian mechanism and therapeutic target for obesity...
  13. pmc Neural dysregulation of peripheral insulin action and blood pressure by brain endoplasmic reticulum stress
    Sudarshana Purkayastha
    Department of Molecular Pharmacology and Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 108:2939-44. 2011
    ..In conclusion, ER stress in the brain represents a mediator of the sympathetic disorders that underlie the development of insulin resistance syndrome and T2D...
  14. pmc Inflammatory cause of metabolic syndrome via brain stress and NF-κB
    Dongsheng Cai
    Department of Molecular Pharmacology and Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Aging (Albany NY) 4:98-115. 2012
    ..This article reviews recent research advances in the neural mechanisms of metabolic syndrome and related diseases from the perspective of pathogenic induction by intracellular stresses and NF-κB pathway of the brain...
  15. doi request reprint Metabolic learning and memory formation by the brain influence systemic metabolic homeostasis
    Yumin Zhang
    1 Department of Molecular Pharmacology, Diabetes Research Center, Institute of Aging, Albert Einstein College of Medicine, Bronx, New York 10461, USA 2 Department of Endocrinology and Metabolism, The First Hospital of Jilin University, Changchun 130021, China
    Nat Commun 6:6704. 2015
    ..In conclusion, our data indicate that the brain, and potentially the hypothalamus, direct metabolic learning and the formation of memories, which contribute to the control of systemic metabolic homeostasis. ..
  16. doi request reprint Neuropeptide exocytosis involving synaptotagmin-4 and oxytocin in hypothalamic programming of body weight and energy balance
    Guo Zhang
    Department of Molecular Pharmacology and Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Neuron 69:523-35. 2011
    ..In conclusion, the negative regulation of synaptotagmin-4 on oxytocin release represents a hypothalamic basis of neuropeptide exocytosis in controlling obesity and related diseases...
  17. pmc Counterbalance between BAG and URX neurons via guanylate cyclases controls lifespan homeostasis in C. elegans
    Tiewen Liu
    Department of Molecular Pharmacology, Institute of Aging, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    EMBO J 32:1529-42. 2013
    ..In conclusion, BAG and URX neurons work as a neural-regulatory system to counterbalance each other via different GCYs to control lifespan homeostasis...
  18. pmc Hypothalamic microinflammation: a common basis of metabolic syndrome and aging
    Yizhe Tang
    Department of Molecular Pharmacology, Diabetes Research Center, Institute of Aging, Albert Einstein College of Medicine, New York, NY 10461, USA
    Trends Neurosci 38:36-44. 2015
    ..Here we summarize recent work and suggest a conceptual model in which hypothalamic microinflammation is a common mediator of metabolic syndrome and aging. ..
  19. ncbi request reprint NFkappaB-mediated metabolic inflammation in peripheral tissues versus central nervous system
    Dongsheng Cai
    Department of Molecular Pharmacology, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Cell Cycle 8:2542-8. 2009
    ..Here, we comparatively review the tissue-specific programs and actions of IKKbeta/NFkappaB in causing and promoting overnutrition-related diseases...
  20. doi request reprint Aberrant miR199a-5p/caveolin1/PPARα axis in hepatic steatosis
    Bo Li
    Shanghai Institute of Endocrine and Metabolic DiseasesShanghai Clinical Center for Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, ChinaDepartment of NeurosurgeryHuashan Hospital of Fudan University, Shanghai 200040, ChinaDepartment of Molecular PharmacologyAlbert Einstein College of Medicine, Bronx, New York 10461, USA
    J Mol Endocrinol 53:393-403. 2014
    ..Upregulated miR199a-5p in hepatocytes may contribute to impaired FA β-oxidation in mitochondria and aberrant lipid deposits, probably via CAV1 and the PPARα pathway. ..