Kafait U. Malik, Ph.D.

Kafait U. Malik, Ph.D.

Professor
Department of Pharmacology


The University of Tennessee Health Science Center
216 Crowe Research Building
874 Union Avenue
Memphis, TN 38163
Phone: (901) 448-6075
Fax: (901) 448-7300
Email: Kafait U. Malik



Education

  • D.Sc. Institution: University of Zagreb, Department of Pharmaceutics, Zagreb, Yugoslavia
  • Ph.D. Institution: University of Sarajevo, Department of Pharmacology, Sarajevo, Yugoslavia
  • Postdoctoral: University of Mainz, Department of Pharmacology, Mainz, W. Germany; University of Ottawa, Department of Pharmacology, Ottawa, Ontario

Link

Research Interests

The objective of the research in this laboratory is to investigate the regulation of adrenergic neuroeffector events in the cardiovascular system. A variety of physiological, pharmacological, cellular and molecular techniques are used to define interaction of these neurohormonal systems in several experimental preparations of different species, both in vitro and in vivo.

The specific aims are: 1) characterization of receptors and the underlying signal transduction mechanisms (coupling of receptors to phospholipases via different G proteins) involved in adrenergically-induced release of arachidonic acid for prostaglandin synthesis; 2) investigation of the mechanism of action of arachidonic acid metabolites on release of the adrenergic transmitter ; and 3) examination of the mechanism of interaction of angiotensins and adrenergic nervous system in the regulation of cardiovascular function.

Representative Publications

  • Tunctan B, Senol SP, Temiz-Resitoglu M, Guden DS, Sahan-Firat S, Falck JR, Malik KU. Eicosanoids derived from cytochrome P450 pathway of arachidonic acid and inflammatory shock. Prostaglandins Other Lipid Mediat. 2019 Dec;145:106377. doi: 10.1016/j.prostaglandins.2019.106377. Epub 2019 Oct 3. Review. PubMed PMID: 31586592.
  • Kocak Z, Temiz-Resitoglu M, Guden DS, Vezir O, Sucu N, Balcı S, Tamer-Gumus L, Tunctan B, Malik KU, Sahan-Firat S. Modulation of oxidative-nitrosative stress and inflammatory response by rapamycin in target and distant organs in rats exposed to hindlimb ischemia-reperfusion: the role of mammalian target of rapamycin. Can J Physiol Pharmacol. 2019 Dec;97(12):1193-1203. doi: 10.1139/cjpp-2019-0394. Epub 2019 Sep 10. PubMed PMID: 31505123.
  • Mukherjee K, Song CY, Estes AM, Dhodi AN, Ormseth BH, Shin JS, Gonzalez FJ, Malik KU. Cytochrome P450 1B1 Is Critical for Neointimal Growth in Wire-Injured Carotid Artery of Male Mice. J Am Heart Assoc. 2018 Sep 18;7(18):e010065. doi: 10.1161/JAHA.118.010065. PubMed PMID: 30371217; PubMed Central PMCID: PMC6222936.
  • Sahan-Firat S, Temiz-Resitoglu M, Guden DS, Senol SP, Sari AN, Cil M, Unsal D, Korkmaz B, Tunctan B, Malik KU, Buharalioglu CK. NF-κB activation mediates LPS-or zymosan-induced hypotension and inflammation reversed by BAY61-3606, a selective Syk inhibitor, in rat models of septic and non-septic shock. Clin Exp Pharmacol Physiol. 2019 Feb;46(2):173-182. doi: 10.1111/1440-1681.13045. PubMed PMID: 30347478.
  • Zou Y, Chen Z, Jennings BL, Zhao G, Gu Q, Bhattacharya A, Cui Y, Yu B, Malik KU, Yue J. Deletion of DGCR8 in VSMCs of adult mice results in loss of vascular reactivity, reduced blood pressure and neointima formation. Sci Rep. 2018 Jan 23;8(1):1468. doi: 10.1038/s41598-018-19660-z. PubMed PMID: 29362439; PubMed Central PMCID: PMC5780492.
  • Song CY, Khan NS, Liao FF, Wang B, Shin JS, Bonventre JV, Malik KU. Brain Cytosolic Phospholipase A2α Mediates Angiotensin II-Induced Hypertension and Reactive Oxygen Species Production in Male Mice. Am J Hypertens. 2018 Apr 13;31(5):622-629. doi: 10.1093/ajh/hpy009. PubMed PMID: 29342227; PubMed Central PMCID: PMC5905655.

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