Open AccessMitochondria and aging: a role for the permeability transition?
Author(s) -
Crompton M.
Publication year - 2004
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1046/j.1474-9728.2003.00073.x
Subject(s) - mitochondrial permeability transition pore , biology , mitochondrion , biophysics , voltage dependent anion channel , cyclophilin , gating , microbiology and biotechnology , permeability (electromagnetism) , membrane permeability , oxidative stress , biochemistry , membrane , programmed cell death , apoptosis , bacterial outer membrane , escherichia coli , gene
Summary When mitochondria are subjected to oxidative stress and relatively high [Ca 2+ ], they undergo a ‘permeability transition’ in which the inner membrane becomes freely permeable to low‐molecular‐weight solutes. This phenomenon reflects reversible deformation of the adenine nucleotide translocase, the loss of its native gating properties and the stabilization of the deformed state by cyclophilin‐D. The permeability transition may be a factor in cell dysfunction associated with aging. This can manifest in a number of ways ranging, in the most severe, from impaired energy transduction and compromised viability to more subtle influences on the propagation of Ca 2+ signals. This article critically examines data relevant to this issue.