Publications by authors named "Mikihiko Nakaoka"

Article Synopsis
  • * An 86-year-old man developed rashes on his foot after undergoing a transcatheter aortic valve replacement, initially suspected to be cholesterol crystal embolization (CCE).
  • * A pathological examination confirmed the rashes were due to HPE, and the patient's condition improved without significant treatment, highlighting the need for awareness of HPE as a potential diagnosis after catheter interventions.
View Article and Find Full Text PDF

Although the direct aortic approach is one option in performing transcatheter aortic valve replacement, it is essential to keep a sheath manually in the same position during the procedure. Holding the sheath by hand is not ideal because of the relatively high dose of radiation to the person who holds the sheath. We here describe a unique way to keep the sheath firm with a table mount system.

View Article and Find Full Text PDF

Alpha-adrenergic agonists is known to be protective in cardiac myocytes from apoptosis induced by beta-adrenergic stimulation. Although there has been a recent focus on the role of cardiac autophagy in heart failure, its role in heart failure with adrenergic overload has not yet been elucidated. In the present study, we investigated the contribution of autophagy to cardiac failure during adrenergic overload both in vitro and in vivo.

View Article and Find Full Text PDF

Background: Diabetic cardiomyopathy is characterized by energetic dysregulation caused by glucotoxicity, lipotoxicity, and mitochondrial alterations. p53 and its downstream mitochondrial assembly protein, synthesis of cytochrome c oxidase 2 (SCO2), are important regulators of mitochondrial respiration, whereas the involvement in diabetic cardiomyopathy remains to be determined.

Methods And Results: The role of p53 and SCO2 in energy metabolism was examined in both type I (streptozotocin [STZ] administration) and type II diabetic (db/db) mice.

View Article and Find Full Text PDF

Inhibition of tumor suppressor p53 is cardioprotective against ischemic injury and provides resistance to subsequent cardiac remodeling. We investigated p53-mediated expansion of ischemic damage with a focus on mitochondrial integrity in association with autophagy and apoptosis. p53(-/-) heart showed that autophagic flux was promoted under ischemia without a change in cardiac tissue ATP content.

View Article and Find Full Text PDF

Bioenergetic homeostasis is altered in heart failure and may play an important role in pathogenesis. p53 has been implicated in heart failure, and although its role in regulating tumorigenesis is well characterized, its activities on cellular metabolism are just beginning to be understood. We investigated the role of p53 and its transcriptional target gene TP53-induced glycolysis and apoptosis regulator (TIGAR) in myocardial energy metabolism under conditions simulating ischemia that can lead to heart failure.

View Article and Find Full Text PDF