David Stowe, MD, PhD
BA, Zoology, Indiana University - Bloomington, IN, 1968
MA, Cell Biology, Indiana University - Bloomington, IN, 1970
PhD, Physiology, Michigan State University - East Lansing, MI, 1974
Postdoc, Cardiac Physiology, University of California - San Francisco, CA, 1974–1976
MD, Medical College of Wisconsin - Milwaukee, WI, 1979-1983
Residency, Anesthesiology, Medical College of Wisconsin - Milwaukee, WI, 1983–1987
- Mechanisms for and protection against cardiac ischemia-reperfusion injury
- Identification and function of mitochondrial ion channels and ion exchangers
- Assessment of mitochondrial transmembrane calcium fluxes and sequestration
- Mitochondrial protection against subacute liver ischemia and traumatic brain injury
(Yang M, Xu Y, Heisner JS, Sun J, Stowe DF, Kwok WM, Camara AKS.) Mitochondrion. 2019 05;46:380-392.
(Haumann J, Camara AKS, Gadicherla AK, Navarro CD, Boelens AD, Blomeyer CA, Dash RK, Boswell MR, Kwok WM, Stowe DF.) Front Physiol. 2018;9:1914.
(Stowe DF, Yang M, Heisner JS, Camara AKS.) J Cardiovasc Pharmacol. 2017 Nov;70(5):314-328.
(Yang M, Camara AKS, Aldakkak M, Kwok WM, Stowe DF.) Biochim Biophys Acta Bioenerg. 2017 Jun;1858(6):442-458.
(Heerdt PM, Stowe DF.) Curr Opin Anaesthesiol. 2017 Feb;30(1):42-49.
(Blomeyer CA, Bazil JN, Stowe DF, Dash RK, Camara AK.) J Bioenerg Biomembr. 2016 06;48(3):175-88.
(Rhodes SS, Camara AK, Aldakkak M, Heisner JS, Stowe DF.) Physiol Rep. 2015 Aug;3(8).
(Lindsay DP, Camara AK, Stowe DF, Lubbe R, Aldakkak M.) Front Physiol. 2015;6:58.
(Abdoli A, Dulikravich GS, Bajaj C, Stowe DF, Jahania MS.) Int J Numer Method Biomed Eng. 2014 Nov;30(11):1372-86.
(Tewari SG, Camara AK, Stowe DF, Dash RK.) J Physiol. 2014 May 01;592(9):1917-30.
(Yang M, Stowe DF, Udoh KB, Heisner JS, Camara AK.) PLoS One. 2014;9(12):e113534.
(Agarwal B, Stowe DF, Dash RK, Bosnjak ZJ, Camara AK.) Front Physiol. 2014;5:341.
The Stowe laboratory is currently active in several areas:
- Mechanism and timing of activation of cardiac mitochondrial small and large K+-sensitive Ca2+ (SKCa and BKCa) channels; their protective role against acute cardiac injury; identification of specific mitochondrial SKCa splice variants in several species, including human; and the molecular and biophysical mechanisms underlying protection by opening of these mitochondrial channels.
- Mitigation of Ca2+ dysregulation and excess reactive oxygen species emission in acute cardiac injury.
- Regulation of mitochondrial Ca2+ flux through Ca2+ channels and Ca2+ exchangers with H+, K+ and Na+; and exploration of dynamic mitochondrial Ca2+ buffering mechanisms.
- Ischemia-induced nitration of nucleotide transporters VDAC and ANT on promoting mitochondrial and cell damage with identification of specific residues that are causative in impeding nucleotide transport and mitochondrial dysfunction.
- Mitochondrial function in liver cells during the perioperative transplant period.
- Mitochondrial function in glial and neurons after subacute tramatic brain injury.
Collaborators include: AKS Camara, WM Kwok, C Pawela, A Geurts, J Hong, MY Yang, J Mishra, Q Cheng, L Keguo, JS Heisner, D Schwabe, and pre- and post doctoral students.