Mitochondrial fission and fusion in human diseases

New England Journal of Medicine

Volumn 370, Issue 11, 2014, Pages 1073-1074

  Sanchis Gomar, Fabian ^a   Derbré, Frederic ^b  

^a UNIVERSITY OF VALENCIA   (Spain)

^b UNIVERSITÉ RENNES 2   (France)

Author keywords

[No Author keywords available]

Indexed keywords

CYTOCHROME C; MITOCHONDRIAL PROTEIN; NUCLEAR RESPIRATORY FACTOR 1; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA COACTIVATOR 1ALPHA; PROTEASOME;

AGING; APOPTOSIS; BIOGENESIS; DISEASE ASSOCIATION; DISORDERS OF MITOCHONDRIAL FUNCTIONS; HEART MUSCLE; HUMAN; LETTER; MITOCHONDRIAL DYNAMICS; MITOCHONDRIAL FISSION; MITOCHONDRIAL FUSSION; MUSCLE MASS; NONHUMAN; NUCLEOTIDE SEQUENCE; OXIDATIVE PHOSPHORYLATION; PRIORITY JOURNAL; PROTEIN EXPRESSION; SARCOPENIA; SKELETAL MUSCLE;

HUMANS; MITOCHONDRIAL DISEASES; MITOCHONDRIAL DYNAMICS; MITOCHONDRIAL PROTEINS;

EID: 84896758882     PISSN: 00284793     EISSN: 15334406     Source Type: Journal    
DOI: 10.1056/NEJMc1316254     Document Type: Letter

References (5)

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4. Derbré F, Gomez-Cabrera MC, Nascimento AL, et al. Age associated low mitochondrial biogenesis may be explained by lack of response of PGC-1α to exercise training. Age (Dordr) 2012;34:669-79.
5. Wenz T, Rossi SG, Rotundo RL, Spiegelman BM, Moraes CT. Increased muscle PGC-1alpha expression protects from sarcopenia and metabolic disease during aging. Proc Natl Acad Sci U S A 2009;106:20405-10.