• By Concept
  • By Last Name
  • By Full Text

Gary M Fiskum

Gary M Fiskum

School of Medicine

Anesthesiology

School of Medicine

Program in Neuroscience

School of Medicine

Biochemistry and Molecular Biology

 BiomedExperts Profile

Directory linkout


Help us refine your profile

Publication Detail

The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.



Mitochondrial mechanisms of neural cell apoptosis.

Brian M Polster; Gary Fiskum (Profiled Authors: Gary M Fiskum; Brian M Polster)

W. Harry Feinstone Department of Microbiology and Molecular Immunology, The Johns Hopkins University School of Public Health, Baltimore, Maryland, USA.
Journal of neurochemistry 2004;90(6):1281-9.

Abstract

The importance of calcium overload, mitochondrial dysfunction, and free radical generation to neuropathological processes has been recognized for many years. Only more recently has evidence accumulated that the programmed cell death process of apoptosis plays an integral role not only in the development of the nervous system, but in the loss of cells following acute neurological insults and chronic disease. In 1996 came the landmark discovery that cytochrome c, an evolutionary old and essential component of the respiratory chain, has a second and deadly function when it escapes the mitochondrion: triggering the cell death cascade. A flurry of activity has since ensued in an effort to understand the mechanistic events associated with mitochondrial permeabilization during apoptosis and regulation by an enigmatic family of proteins characterized by homology to the proto-oncogene Bcl-2. This review discusses the evidence for various release mechanisms of apoptotic proteins (e.g. cytochrome c) from neural cell mitochondria, focusing particularly on roles for calcium, Bax, p53, and oxidative stress. The need for new drugs that act at the level of the mitochondrion to prevent apoptosis is also highlighted.

5 Originating Grant

Scientific Context

This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.

Related Publications