Abdul H. Khan
Associate Staff Scientist
Also affiliated: Tulane University (2008–2011); Bahauddin Zakariya University (2008–2009); Froedtert Hospital (2016–2020); United States Department of Veterans Affairs (1981–1985); Ochsner Health System (2013); Universiti Sains Malaysia (2007–2010); University of South Carolina (1981–1984); Islamia University of Bahawalpur (2017); Bangladesh Medical University (2025); Czech Academy of Sciences (2013); University of California, Irvine (2007); Medical College of Wisconsin (1985–2024); Columbia University Irving Medical Center (2010); Ochsner Medical Center (2010); Veterans Health Administration (1985); Tulane Medical Center (2010); Wm. Jennings Bryan Dorn VA Medical Center (1982); Chase Farm Hospital (2011); Henry Ford Hospital (2013); Columbia VA Health Care System (1982); Milwaukee VA Medical Center (2012–2014); Mayo Clinic Health System (2021); Czech Academy of Sciences, Institute of Physiology (2013); Medical College of Wisconsin Cancer Center (2021); Albany Medical College (1994); Case Western Reserve University (2013); University of Missouri (2024); The University of Texas Southwestern Medical Center (2013); American University of Antigua (2025); University of Colorado Denver (2010); Dhaka Medical College and Hospital (2024)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Dr. Abdul H. Khan's research focuses on preclinical drug development, with a particular emphasis on integrative physiology, pharmacology, and in vivo preclinical and translational research. His work investigates therapeutic strategies for cardiovascular and renal diseases, as well as anti-fibrotic drug development. Recent studies have explored the potential of specific molecules, such as the kidney-targeted epoxyeicosatrienoic acid analog EET-F01, to reduce inflammation and oxidative stress in cases of cisplatin-induced nephrotoxicity. He has also examined the impact of chloride channel 6 (CLC-6) loss on vascular smooth muscle contractility and arterial stiffness, and investigated the efficacy of the multitarget molecule PTUPB in treating diabetic nephropathy in rats.
Further research by Dr. Khan and his collaborators has delved into the effects of environmental factors on health, including the reproductive toxicity of polystyrene microplastics in male mice. His group has also studied sex differences in kidney injury following unilateral ureteral obstruction in mice, and the therapeutic potential of dual soluble epoxide hydrolase inhibitor–farnesoid X receptor agonist treatments for renal inflammation and fibrosis. Dr. Khan has authored or co-authored 193 publications, with a Google Scholar H-index of 31, and has received recognition as a highly cited researcher. He also leads a research group and has a background in biomedical education and clinical research.
Metrics
- h-index: 31
- Publications: 187
- Citations: 3,202
Positions
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Associate Staff Scientist 2024–presentUniversity of Arkansas for Medical Sciences Pharmaceutical Sciences ORCID
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Assistant Professor 2023–2024University of Missouri Physiology, Pharmacology, Anesthesiology ORCID
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Instructor 2022–2023University of Tennessee Health Science Center Physiology ORCID
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Assistant Professor 2014–2021Medical College of Wisconsin Pharmacology and Toxicology ORCID
Selected Publications
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Sorafenib Treatment Results in Greater Kidney Injury in Renal Hypoplasia Mice (Abstract ID: 272359) (2026)
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Renal hemodynamics underlie hepatorenal physiology in bile duct-ligated rats (2026)
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Renoprotective approaches against anthracycline nephrotoxicity (2026)
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EET-Based Therapeutics Mitigate Sorafenib-Associated Glomerular Cell Damage (2025)
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Dual acting inhibitor of soluble epoxide hydrolase and Cyclooxygenase-2, attenuates glomerular injury in renal hypoplasia mice (2025)
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Transforming growth factor β receptor 1 and mitogen-activated protein 4 kinase 4 dual inhibitor, TK-850, reduces renal fibrosis in unilateral ureteral–obstructed mice (2025)
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591 Low kidney mass contributes to enhanced fractionated irradiation-induced renal hemodynamic dysfunction in mice (2025)
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Editorial: Debates in experimental pharmacology and drug discovery 2023: innovative approaches to chronic kidney disease drug discovery, identification of targets and safety assessment (2025)
Collaboration Network
Top Collaborators
- Dual acting inhibitor of soluble epoxide hydrolase and Cyclooxygenase-2, attenuates glomerular injury in renal hypoplasia mice
- Editorial: Debates in experimental pharmacology and drug discovery 2023: innovative approaches to chronic kidney disease drug discovery, identification of targets and safety assessment
- Renal hemodynamics underlie hepatorenal physiology in bile duct-ligated rats
- 591 Low kidney mass contributes to enhanced fractionated irradiation-induced renal hemodynamic dysfunction in mice
- Transforming growth factor β receptor 1 and mitogen-activated protein 4 kinase 4 dual inhibitor, TK-850, reduces renal fibrosis in unilateral ureteral–obstructed mice
Showing 5 of 7 shared publications
- Dual acting inhibitor of soluble epoxide hydrolase and Cyclooxygenase-2, attenuates glomerular injury in renal hypoplasia mice
- Renoprotective approaches against anthracycline nephrotoxicity
- Renal hemodynamics underlie hepatorenal physiology in bile duct-ligated rats
- 591 Low kidney mass contributes to enhanced fractionated irradiation-induced renal hemodynamic dysfunction in mice
- Transforming growth factor β receptor 1 and mitogen-activated protein 4 kinase 4 dual inhibitor, TK-850, reduces renal fibrosis in unilateral ureteral–obstructed mice
Showing 5 of 6 shared publications
- 591 Low kidney mass contributes to enhanced fractionated irradiation-induced renal hemodynamic dysfunction in mice
- Transforming growth factor β receptor 1 and mitogen-activated protein 4 kinase 4 dual inhibitor, TK-850, reduces renal fibrosis in unilateral ureteral–obstructed mice
- EET-Based Therapeutics Mitigate Sorafenib-Associated Glomerular Cell Damage
- 591 Low kidney mass contributes to enhanced fractionated irradiation-induced renal hemodynamic dysfunction in mice
- Transforming growth factor β receptor 1 and mitogen-activated protein 4 kinase 4 dual inhibitor, TK-850, reduces renal fibrosis in unilateral ureteral–obstructed mice
- Dual acting inhibitor of soluble epoxide hydrolase and Cyclooxygenase-2, attenuates glomerular injury in renal hypoplasia mice
- Renal hemodynamics underlie hepatorenal physiology in bile duct-ligated rats
- Dual acting inhibitor of soluble epoxide hydrolase and Cyclooxygenase-2, attenuates glomerular injury in renal hypoplasia mice
- Renal hemodynamics underlie hepatorenal physiology in bile duct-ligated rats
- Editorial: Debates in experimental pharmacology and drug discovery 2023: innovative approaches to chronic kidney disease drug discovery, identification of targets and safety assessment
- Editorial: Debates in experimental pharmacology and drug discovery 2023: innovative approaches to chronic kidney disease drug discovery, identification of targets and safety assessment
- 591 Low kidney mass contributes to enhanced fractionated irradiation-induced renal hemodynamic dysfunction in mice
- 591 Low kidney mass contributes to enhanced fractionated irradiation-induced renal hemodynamic dysfunction in mice
- Transforming growth factor β receptor 1 and mitogen-activated protein 4 kinase 4 dual inhibitor, TK-850, reduces renal fibrosis in unilateral ureteral–obstructed mice
- Transforming growth factor β receptor 1 and mitogen-activated protein 4 kinase 4 dual inhibitor, TK-850, reduces renal fibrosis in unilateral ureteral–obstructed mice
- Dual acting inhibitor of soluble epoxide hydrolase and Cyclooxygenase-2, attenuates glomerular injury in renal hypoplasia mice
- Dual acting inhibitor of soluble epoxide hydrolase and Cyclooxygenase-2, attenuates glomerular injury in renal hypoplasia mice
- Dual acting inhibitor of soluble epoxide hydrolase and Cyclooxygenase-2, attenuates glomerular injury in renal hypoplasia mice
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