Carlos Bernal-Mizrachi

Philip E & Carolyn E Cryer Professor of Medicine, Professor of Cell Biology and Physiology

    • 2976 Citations
    19992020

    Research output per year

    If you made any changes in Pure these will be visible here soon.

    Personal profile

    Research interests

    The goal of my laboratory is to pursue a series of studies focused mainly on two mechanisms that we believe are critical to the pathophysiology of cardiovascular disease in patients with Type 2 DM and prediabetes: Vitamin D deficiency and tissue glucocorticoid excess. Patients with prediabetes and Type 2 DM have a higher prevalence of vitamin D deficiency and hypertension compared to the general population. Animal and human studies have shown that vitamin D improves peripheral insulin action, suppresses the renin-angiotensin system and decreases vascular inflammatory factors; mechanisms responsible for increased blood pressure (BP). However, there is lack of evidence as to whether the increased prevalence of hypertension and atherosclerosis in patients with diabetes or pre-diabetes is truly influenced by vitamin D deficiency. Our laboratory is using multiple animal models, novel molecular biology techniques and clinical trials to assess whether alterations in the expression of genes related to vitamin D metabolism are responsible for the development of these diseases. Adipose and hepatic glucocorticoid excess in mice resembles metabolic syndrome, a poorly understood condition characterized by insulin resistance, chronic inflammation and cardiovascular disease. We are interested to find the mechanisms by which glucocorticoids induce hypertension and atherosclerosis. In the past, we have demonstrated that a nuclear transcription factor PPAR a (important for lipid metabolism), and hepatic afferent vagal nerve activation are required for glucocorticoid-induced hypertension and diabetes in mice. Now, we are using genetically engineered mice and classical physiology to characterize the interaction between lipid metabolism and glucocorticoid signaling in critical tissues responsible for the development of atherosclerosis. Identifying these mechanisms may lead to the development of novel therapies for the treatment of diabetes and cardiovascular disease.

    Areas of Clinical Interest

    Endocrinology, diabetes, metabolism

    Fingerprint Dive into the research topics where Carlos Bernal-Mizrachi is active. These topic labels come from the works of this person. Together they form a unique fingerprint.

    • 6 Similar Profiles

    Network Recent external collaboration on country level. Dive into details by clicking on the dots.

    Research Output

    Immunity and Hypertension

    Zhang, R. M., McNerney, K. P., Riek, A. E. & Bernal-Mizrachi, C., 2020, (Accepted/In press) In : Acta Physiologica.

    Research output: Contribution to journalReview article

  • 1 Scopus citations
  • 1 Scopus citations

    Deletion of JNK2 prevents vitamin-D-deficiency-induced hypertension and atherosclerosis in mice

    Oh, J., Riek, A. E., Zhang, R. M., Williams, S. A. S., Darwech, I. & Bernal-Mizrachi, C., Mar 2018, In : Journal of Steroid Biochemistry and Molecular Biology. 177, p. 179-186 8 p.

    Research output: Contribution to journalArticle

  • 6 Scopus citations
  • 6 Scopus citations

    Vitamin D and the Cardiovascular System

    Riek, A. E., Rajagopal, R. & Bernal-Mizrachi, C., Jan 1 2018, Biochemistry, Physiology and Diagnostics. Elsevier Inc., Vol. 1. p. 545-562 18 p.

    Research output: Chapter in Book/Report/Conference proceedingChapter

  • 1 Scopus citations