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Mitochondrial biogenesis in neurodegeneration
Author(s) -
Li P. Andy,
Hou Xiaolin,
Hao Shaocai
Publication year - 2017
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.24042
Subject(s) - tfam , mitochondrial biogenesis , nrf1 , mitochondrion , microbiology and biotechnology , biology , neurodegeneration , organelle biogenesis , programmed cell death , dnaja3 , transcription factor , mitochondrial dna , coactivator , mitochondrial fusion , biogenesis , apoptosis , biochemistry , medicine , disease , gene
Mitochondria play a key role in energy production, calcium homeostasis, cell survival, and death. Adverse stimulations including neurodegenerative diseases may result in mitochondrial dynamic imbalance, free radical production, calcium accumulation, intrinsic cell death pathway activation and eventually cell death. Therefore, preserving or promoting mitochondrial function is a potential therapeutic target for the treatment of neurodegenerative disorders. Mitochondrial biogenesis is a process by which new mitochondria are produced from existing mitochondria. This biogenesis process is regulated by Peroxisome proliferator‐activated receptor‐gamma (PPARγ) coactivator‐1alpha (PGC‐1α). Once being activated by either phosphorylation or de‐acetylation, PGC‐1α activates nuclear respiratory factor 1 and 2 (NRF1 and NRF2), and subsequently mitochondrial transcription factor A (Tfam). The activation of this PGC‐1α ‐ NRF –Tfam pathway leads to synthesis of mitochondrial DNA and proteins and generation of new mitochondria. © 2017 Wiley Periodicals, Inc.