Martin Bienengraeber, PhD
Adjunct Professor
Locations
- Pharmacology and Toxicology
Contact Information
General Interests
Cardiovascular Pharmacology
Education
PhD, Chemistry, University of Munich, 1990
Research Interests
Mitochondria constitute the core of cellular energy metabolism as the site of the greatest ATP production. In addition, they play an important role in regulating ionic homeostasis of the cell. It has been suggested that mitochondrial dysfunction may be the major cause for tissue injury during cardiac ischemia and reperfusion. On the other hand, they present a valuable target for triggering protective mechanisms. Exposure of the heart to volatile anesthetics like isoflurane before or after an ischemic event helps to maintain cellular and mitochondrial function in the whole heart, in cardiomyocytes and in isolated mitochondria. One of my research interests revolves around the role of mitochondria as triggers and effectors in protection of the heart from ischemia and stress. We use physiological, pharmacological and molecular techniques as well as proteomics to demonstrate quantifiable alterations in mitochondrial bioenergetics and protein expression during or after exposure to volatile anesthetics.
In a project which in May 2010 received NIH R01 funding, we study the impact of far red/near infrared light (670 nm) on the heart and mitochondria during cardiac ischemia and reperfusion injury. Exposure of the ischemic heart with a LED light source at the time of reperfusion turns out to reduce injury. Mitochondria may play a crucial role in the mechanism behind this phenomenon. In addition, nitric oxide from unconventional sources such as myoglobin or hemoglobin is involved. Projects are performed in collaboration with investigators from the Anesthesiology, the Pharmacology and Toxicology, the Physiology and the Biophysics department.
While the cardioprotective strategies we are studying are extremely powerful in healthy, young animals, diseases such as diabetes diminish their efficacy and limit clinical applicability. Therefore, in collaboration the MCW Human and Molecular Genetics center we examine a rat model of diabetes with mutations in the mitochondrial DNA, which produces a diabetic phenotype as a background for evaluating cardioprotective mechanisms. Interestingly, near infrared light still protects against cardiac ischemia and reperfusion injury during diabetes.
In a project which in May 2010 received NIH R01 funding, we study the impact of far red/near infrared light (670 nm) on the heart and mitochondria during cardiac ischemia and reperfusion injury. Exposure of the ischemic heart with a LED light source at the time of reperfusion turns out to reduce injury. Mitochondria may play a crucial role in the mechanism behind this phenomenon. In addition, nitric oxide from unconventional sources such as myoglobin or hemoglobin is involved. Projects are performed in collaboration with investigators from the Anesthesiology, the Pharmacology and Toxicology, the Physiology and the Biophysics department.
While the cardioprotective strategies we are studying are extremely powerful in healthy, young animals, diseases such as diabetes diminish their efficacy and limit clinical applicability. Therefore, in collaboration the MCW Human and Molecular Genetics center we examine a rat model of diabetes with mutations in the mitochondrial DNA, which produces a diabetic phenotype as a background for evaluating cardioprotective mechanisms. Interestingly, near infrared light still protects against cardiac ischemia and reperfusion injury during diabetes.