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

  • Tan XL, Xue YQ, Ma T, Wang X, Li JJ, Lan L, Malik KU, McDonald MP, Dopico AM, Liao FF. Partial eNOS deficiency causes spontaneous thrombotic cerebral infarction, amyloid angiopathy and cognitive impairment. Mol Neurodegener. 2015 Jun 24;10:24. doi: 10.1186/s13024-015-0020-0. PubMed PMID: 26104027; PubMed Central PMCID: PMC4479241.
  • Khan NS, Song CY, Thirunavukkarasu S, Fang XR, Bonventre JV, Malik KU. Cytosolic Phospholipase A2α Is Essential for Renal Dysfunction and End-Organ Damage Associated With Angiotensin II-Induced Hypertension. Am J Hypertens. 2015 Jun 4. pii: hpv083. [Epub ahead of print] PubMed PMID: 26045535.
  • Pingili AK, Kara M, Khan NS, Estes AM, Lin Z, Li W, Gonzalez FJ, Malik KU. 6β-hydroxytestosterone, a cytochrome P450 1B1 metabolite of testosterone, contributes to angiotensin II-induced hypertension and its pathogenesis in male mice. Hypertension. 2015 Jun;65(6):1279-87. doi: 10.1161/HYPERTENSIONAHA.115.05396. Epub 2015 Apr 13. PubMed PMID: 25870196; PubMed Central PMCID: PMC4433413.
  • Jennings BL, Moore JA, Pingili AK, Estes AM, Fang XR, Kanu A, Gonzalez FJ, Malik KU. Disruption of the cytochrome P-450 1B1 gene exacerbates renal dysfunction and damage associated with angiotensin II-induced hypertension in female mice. Am J Physiol Renal Physiol. 2015 May 1;308(9):F981-92. doi: 10.1152/ajprenal.00597.2014. Epub 2015 Feb 18. PubMed PMID: 25694484; PubMed Central PMCID: PMC4420992.
  • Khan NS, Song CY, Jennings BL, Estes AM, Fang XR, Bonventre JV, Malik KU. Cytosolic phospholipase A2α is critical for angiotensin II-induced hypertension and associated cardiovascular pathophysiology. Hypertension. 2015 Apr;65(4):784-92. doi: 10.1161/HYPERTENSIONAHA.114.04803. Epub 2015 Feb 9. PubMed PMID: 25667212; PubMed Central PMCID: PMC4359078.
  • Sari AN, Korkmaz B, Serin MS, Kacan M, Unsal D, Buharalioglu CK, Sahan Firat S, Manthati VL, Falck JR, Malik KU, Tunctan B. Effects of 5,14-HEDGE, a 20-HETE mimetic, on lipopolysaccharide-induced changes in MyD88/TAK1/IKKβ/IκB-α/NF-κB pathway and circulating miR-150, miR-223, and miR-297 levels in a rat model of septic shock. Inflamm Res. 2014 Sep;63(9):741-56. doi: 10.1007/s00011-014-0747-z. Epub 2014 Jun 12. PubMed PMID: 24915805; PubMed Central PMCID: PMC4158117.

View more references (pubmed link)