Education & Training
- Graduate School – University of Alabama – PhD – Cellular & Molecular Pathology
NIH Grants: R01, P01
Dr. Shiva’s research focuses broadly on understanding the mechanisms by which mitochondrial function is regulated, particularly by reactive oxygen and nitrogen species and the contribution of these mechanisms to cardiovascular health and disease pathogenesis. Using a wide spectrum of techniques ranging from the biochemical study of isolated mitochondria to whole animal models and measurement of bioenergetic function in human blood cells, the Shiva lab is currently engaged in a number of active projects along two major scientific themes. On a basic research level, Dr. Shiva’s lab is interested in the mechanisms by which reactive nitrogen species (nitric oxide, nitrite) and heme proteins (hemoglobin and myoglobin) regulate mitochondrial function. Dr. Shiva’s work has demonstrated that in the heart, reactions of nitrite and myoglobin are crucial to protecting mitochondria, leading to preservation of heart tissue after ischemia/reperfusion. In contrast, her work has shown that in hemolytic disease such as Sickle Cell Disease, free hemoglobin damages platelet mitochondria, ultimately leading to platelet dysfunction and thrombosis. On a more clinical/translational level, Dr. Shiva has optimized methodology to measure bioenergetics in human platelets and is currently utilizing this technique to test whether platelets can be used a biomarker for mitochondrial changes in human disease as well as whether this measure can be used as a prognostic indicator.
- Dezfulian C, Taft M, Corey C, Hill G, Krehel N, Rittenberger JC, Guyette FX, Shiva S. Biochemical signaling by remote ischemic conditioning of the arm versus thigh: Is one raise of the cuff enough? Redox Biol. 2017 Aug;12:491-498. doi: 10.1016/j.redox.2017.03.010. Epub 2017 Mar 18. PubMed PMID: 28334684; PubMed Central PMCID: PMC5362138.
- Nguyen QL, Corey C, White P, Watson A, Gladwin MT, Simon MA, Shiva S. Platelets from pulmonary hypertension patients show increased mitochondrial reserve capacity. JCI Insight. 2017 Mar 9;2(5):e91415. doi: 10.1172/jci.insight.91415. PubMed PMID: 28289721; PubMed Central PMCID: PMC5333965.
- Cardenes N, Corey C, Geary L, Jain S, Zharikov S, Barge S, Novelli EM, Shiva S. Platelet bioenergetic screen in sickle cell patients reveals mitochondrial complex V inhibition, which contributes to platelet activation. Blood. 2014 May 1;123(18):2864-72. doi: 10.1182/blood-2013-09-529420. Epub 2014 Mar 27. PubMed PMID: 24677541; PubMed Central PMCID: PMC4007612.
- Kamga Pride C, Mo L, Quesnelle K, Dagda RK, Murillo D, Geary L, Corey C, Portella R, Zharikov S, St Croix C, Maniar S, Chu CT, Khoo NK, Shiva S. Nitrite activates protein kinase A in normoxia to mediate mitochondrial fusion and tolerance to ischaemia/reperfusion. Cardiovasc Res. 2014 Jan 1;101(1):57-68. doi: 10.1093/cvr/cvt224. Epub 2013 Sep 30. PubMed PMID: 24081164; PubMed Central PMCID: PMC3868348.
- de Lima Portella R, Lynn Bickta J, Shiva S. Nitrite Confers Preconditioning and Cytoprotection After Ischemia/Reperfusion Injury Through the Modulation of Mitochondrial Function. Antioxid Redox Signal. 2015 Aug 1;23(4):307-27. doi: 10.1089/ars.2015.6260. Review. PubMed PMID: 26094636.
- Xu W, Cardenes N, Corey C, Erzurum SC, Shiva S. Platelets from Asthmatic Individuals Show Less Reliance on Glycolysis. PLoS One. 2015 Jul 6;10(7):e0132007. doi: 10.1371/journal.pone.0132007. eCollection 2015. PubMed PMID: 26147848; PubMed Central PMCID: PMC4492492.