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Биография

Dr. Naik begin his scientific career earning a Master’s degree in Exercise Physiology from the University of Wisconsin – Milwaukee. This work focused on determining the cellular mechanisms mediating functional hyperemia in skeletal muscle.  He continued to pursue his interest in cardiovascular physiology at the University of New Mexico School of Medicine, earning a PhD in Biomedical Sciences where he investigated the signaling pathway mediating vasodilation in response to heme oxygenase-derived carbon monoxide. Dr. Naik completed his postdoctoral training at the University of Mississippi School of Medicine where his research investigated the vascular dysfunction associated with obesity and metabolic syndrome. Dr. Naik joined the faculty of the UNM SOM Department of Cell Biology and Physiology in 2011.

Области специализации

  • Сердечно-сосудистая физиология
  • микроциркуляции

Ключевые публикации

  • Zhang B, Paffett ML, Naik JS, Jernigan NL, Walker BR, Resta TC. Cholesterol Regulation of Pulmonary Endothelial Calcium Homeostasis. Curr Top Membr. 2018;82:53-91. doi: 10.1016/bs.ctm.2018.09.001. Epub 2018 Oct 8. PMID: 30360783.
  • Naik JS, Osmond JM, Walker BR, Kanagy NL. Hydrogen sulfide-induced vasodilation mediated by endothelial TRPV4 channels. Am J Physiol Heart Circ Physiol. 2016 Dec 1;311(6):H1437-H1444. doi: 10.1152/ajpheart.00465.2016. Epub 2016 Oct 7. PMID: 27765747; PMCID: PMC5206343.
  • Zhang B, Naik JS, Jernigan NL, Walker BR, Resta TC. Reduced membrane cholesterol limits pulmonary endothelial Ca2+ entry after chronic hypoxia. Am J Physiol Heart Circ Physiol. 2017 Jun 1;312(6):H1176-H1184. doi: 10.1152/ajpheart.00097.2017. Epub 2017 Mar 31. PMID: 28364016; PMCID: PMC5495930.
  • Jernigan NL, Naik JS, Weise-Cross L, Detweiler ND, Herbert LM, Yellowhair TR, Resta TC. Contribution of reactive oxygen species to the pathogenesis of pulmonary arterial hypertension. PLoS One. 2017 Jun 30;12(6):e0180455. doi: 10.1371/journal.pone.0180455. PMID: 28666030; PMCID: PMC5493402.
  • Naik JS, Walker BR. Endothelial-dependent dilation following chronic hypoxia involves TRPV4-mediated activation of endothelial BK channels. Pflugers Arch. 2018 Apr;470(4):633-648. doi: 10.1007/s00424-018-2112-5. Epub 2018 Jan 29. PMID: 29380056; PMCID: PMC5854740.

 

Пол

M

Языки

  • Английский

Исследования

Dr Naik’s research focuses on understanding the cellular mechanisms by which endothelial and vascular smooth muscle cells communicate in order to regulated blood flow to meet the metabolic demands of body organs. His most recent work has focused on the role of endothelial-derived gaseous signaling molecules, carbon monoxide and hydrogen sulfide in endothelial-dependent dilation as well as the role of calcium microdomains in ion channel activation. His work was the first to demonstrate that H2S-induced vasodilation involves TRPV4 channels through the formation of Ca2+-sparklets and strengthens our previous observation that a novel endothelial Ca2+-activated large conductance calcium activated K+ channels participate in vasodilation in small mesenteric arteries.

Курсы обучения

  • Pulmonary Physiology Phase 1 Medical Curriculum
  • BIOM 510 - Physiology
  • BIOM 657 - Advanced Cellular and Systems Physiology
  • BIOM 659 - Seminar: Cardiovascular Biology