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. Author manuscript; available in PMC: 2011 Oct 1.
Published in final edited form as: Circ Res. 2010 Oct 1;107(7):825–838. doi: 10.1161/CIRCRESAHA.110.223818

Table 1.

Cardiac and energetic phenotypes of transgenic and knockout mouse models.

Transcription Factor
or coactivator
Gain-of-function
cardiac phenotype
Loss-of-function
cardiac phenotype
References
PPARα ⇑FAO, lipotoxicity, HF-
induced CM, ⇓-tolerance
to I/R
Mild. Resistance to
I/R, ⇓work capacity
83-87, 192
PPARβ/δ ⇑glucose utilization,
resistance to I/R,
⇑glycogen content
⇓FAO, lipotoxic CM,
early lethality
81, 89, 90
PPARγ Lipotoxic CM Cardiac hypertrophy 91, 92
ERRα ND ⇓respiratory
efficiency, ⇓PCr,
TAC-induced CM
154
ERRγ ND Perinatal lethality 68, 69
TFAM Protects from MI
induced heart failure
Spontaneous CM 77-79
PGC-1α ⇑mitochondrial
proliferation, reversible
CM
Energy deficiency
(⇓ATP, ⇓PCr),
TAC-induced CM,
⇓work capacity
16, 49, 52, 153, 157
PGC-1β ND Mild energy
deficiency, Perinatal
lethality and
mitochondrial
dysfunction when
combined with PGC-
1α KO
163-165