Paul Sanders MD
Research Scientist, Birmingham VA Health Care System | Professor of Medicine and Cell, Developmental and Integrative Biology, University of Alabama at Birmingham
VA Birmingham health care
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Personal Statement
Dr. Sanders is a physician scientist who began his bench research program during his nephrology fellowship. For the past 35 years, he has received and managed extramural funding from the National Institutes of Health and Department of Veterans Affairs. His laboratory focuses on how protein-protein interactions and redox signaling events produce clinical kidney injury through inflammation and fibrosis in the setting of monoclonal gammopathies, during the development of hypertension-associated kidney injury, and disease processes that lead to progressive loss of kidney function. Dr. Sanders remains an active clinician who manages patients at all stages of their kidney disease, and his patients serve as a source of inspiration and motivation and further inform his research activities. Specifically, Dr. Sanders performs pre-clinical research and collaborates on clinical studies designed to determine 1) redox signaling mechanisms by which dietary sodium and potassium alter endothelial function and vascular stiffness; 2) the pathogenesis of kidney diseases associated with immunoglobulin light chains, 3) mechanisms of salt sensitivity, salt-sensitive hypertension and hypertension-induced kidney injury, and 4) mechanisms of kidney disease progression.
Education
- BS, University of Alabama in Huntsville, Huntsville, AL
- MD, University of South Alabama, Mobile, AL
- Internship, University of Alabama Hospital, Birmingham, AL
- Residency, University of Alabama Hospital, Birmingham, AL
- Fellowship, Nephrology, University of Alabama Hospital, Birmingham, AL
Research Interests
- Investigating mechanisms of salt-sensitive hypertension and hypertension-induced kidney injury
- Defining the role of dietary sodium and potassium on endothelial function and vascular stiffness
- A lasting interest in determining how monoclonal immunoglobulins produce kidney injury
- Limiting the progression of chronic kidney disease
Recent Publications
- Feng W, Guan Z, Xing D, Li X, Ying W-Z, Remedies CE, Inscho EW, Sanders PW: Avian Erythroblastosis Virus E26 Oncogene Homolog-1 (ETS-1) plays a role in renal microvascular pathophysiology in the Dahl salt-sensitive rat. Kidney Int. 97:528-537, 2020. PMCID: PMC7039742
- Upadhyay R, Ying W-Z, Nasrin Z, Safah H, Jaimes EA, Feng W, Sanders PW*, Batuman V*: Free light chains injure proximal tubule cells through STAT1-HMGB1-TLR axis. JCI Insight 2020 5(14):137191. doi:10.1172/jci.insight.137191 *contributed equally to the work. PMCID: PMC7453901
- Ying Ke, Feng W, Ying W-Z, Sanders PW: Cellular antioxidant mechanisms control immunoglobulin light chain-mediated proximal tubule injury. Free Radic Biol Med 171:80-90, 2021. PMCID: PMC8217262
- Feng W, Ying W-Z, Li X, Curtis LM, Sanders PW: Renoprotective effect of Stat1 deletion in murine aristolochic acid nephropathy. Am. J. Physiol. Renal Physiol. 320:F87-F96, 2021. PMCID: PMC7847048
- Ying W-Z, Li X, Rangarajan S, Feng W, Curtis LM, Sanders PW: Immunoglobulin light chains generate pro-inflammatory and pro-fibrotic kidney injury. J. Clin. Invest. 129:2792-2806, 2019. PMCID: PMC6597222 (Paper selected by the Editorial Board for accompanying commentary.)
- A full list of published works is available at http://www.ncbi.nlm.nih.gov/pubmed/?term=sanders+pw