Chapters authored
Mitochondrial Trafficking by Prohibitin-Kinesin-Myosin- Cadherin Complex in the Eye
Disruption of the mitochondrial-nuclear network leads to accelerated aging and age-related diseases, including age-related macular degeneration. The current study tested the hypothesis that mitochondrial morphology could be demonstrated quantitatively using a mathematic model and mitochondrial trafficking complex under stress conditions. To test our hypothesis, normal and aberrant mitochondria were examined quantitatively based on mitochondrial size, shape, position, composition, and dynamics. Adaptation of the mitochondrial network to changes in the intracellular oxidation and reduction milieu is critical for the survival of retinal pigment epithelial cells. Our mitochondrial interactome mapping demonstrated that a positive correlation may exist between oxidative stress-mediated phosphorylation and age-related disease progression. The current interactome may provide a potential therapeutic approach to treat mitochondria-induced neurodegeneration, including age-related macular degeneration.
Part of the book: Mitochondrial Diseases
Nitric Oxide and Oxidative Stress-Mediated Cardiovascular Functionality: From Molecular Mechanism to Cardiovascular Disease
The underlying pathology of most cardiovascular diseases (CVDs) such as coronary artery disease, high blood pressure, and stroke involves decreased cardiovascular contractility and anatomic alterations in cardiovascular structures. Nitric oxide (NO) regulates vascular tone and contractile function of myocardium and maintains blood vessel homeostasis. Interestingly, the effect of NO is like a double-edged sword in the body. Insufficient NO causes hypertension and atherosclerosis, while an overproduction of NO may foster inflammation and cause heart infarction and shock. In addition, growing evidences have shown that oxidative stress plays pivotal roles in the initiation and progression of CVDs. This chapter will discuss in detail the roles NO plays in the cardiovascular system under both physiological and pathological conditions. We will focus on: (1) the molecular mechanism of cardiovascular contraction, (2) NO/Ca2+-induced muscle relaxation, (3) NO-related structural change in blood vessels, and (4) redox balance in the cardiovascular system. The relationships between these molecular mechanisms and the characteristics of CVDs will be highlighted.
Part of the book: Vascular Biology