NDLI: Inner mitochondrial maxi-Kâº channels in neonatal renal tubular cells: novel therapeutic targets to control apoptosis.

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Inner mitochondrial maxi-Kâº channels in neonatal renal tubular cells: novel therapeutic targets to control apoptosis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kazama, Itsuro Maruyama, Yoshio
Description	Country affiliation: Japan Author Affiliation: Kazama I ( Department of Physiology I, Tohoku University Graduate School of Medicine, Seiryo-cho, Aoba-ku, Sendai, Miyagi, Japan. kazaitsu@med.tohoku.ac.jp)
Abstract	In developing kidneys, the total cell population is partly regulated by apoptosis. Despite our understanding of the molecular involvement in the regulatory pathway of apoptosis, we know little about the physiological involvement. Cardiomyocytes express large conductance voltage- and Ca(2+)-activated K(+) (maxi-K(+)) channels in their inner mitochondrial membranes. Triggering the mitochondrial K(+) influx necessary to inhibit apoptosis, the channels play cytoprotective roles during ischemic injury. Since proximal tubular cells in neonatal kidneys are physiologically under hypoxic stress, and since the channel activity is stimulated by hypoxia, those cells would share the same regulatory mechanism of apoptosis with ischemic cardiomyocytes. Therefore, we hypothesize here that the proximal tubular cells in neonatal kidneys would also express the maxi-K(+) channels in their inner mitochondrial membranes, and that the channels would play regulatory roles in apoptosis. Our hypothesis is unique because it sheds light for the first time on a physiological mechanism that involves the mitochondrial membranes in developing kidneys. It is also important because the idea could have novel therapeutic implications for kidney diseases that are associated with apoptosis.
File Format	HTM / HTML
ISSN	03069877
Issue Number	6
Volume Number	78
e-ISSN	15322777
Journal	Medical Hypotheses
Language	English
Publisher	Elsevier
Publisher Date	2012-06-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Medical theory Apoptosis Physiology Kidney Tubules, Proximal Metabolism Kidney Growth & Development Large-conductance Calcium-activated Potassium Channels Mitochondrial Membranes Animals Drug Effects Humans In Situ Nick-end Labeling Infant, Newborn Mice Patch-clamp Techniques Methods Potassium Journal Article
Content Type	Text
Resource Type	Article
Subject	Medicine

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