Table 2.

Genetic models of DCM and related cardiac responses.

	Upregulation							Downregulation
	PPARα	PPARγ	LCACS1	LPL	FATP1	PKCβ	UCPDTA	CIRKO	GLUT4	ATGL	PDK1	PI3K	GCK
Heart failure markers	↑ANP, BNP	↑ANP, BNP	↑ANP, BNP	↑ANP, BNP					↑ANP, BNP			↑ANP, BNP
Cardiac abnormalities
Functional
Diastolic function	↓	↓	↓	↓	↓	↓	↓	↓	↓/~	↓	↓	↓	↓
Systolic function	↓	↓	↓	↓	~	↓	~	↓	↓/~	↓	↓	~
Structural
Hypertrophy	↑	↑	↑	↑	↑	↑	↑	↓	↑	↑	↑	↑	↑
Inflammation						↑				~
Fibrosis	↑		↑	↑	↑	↑	↑	~	↑/~	↑	↑	↑	↑
Steatosis	↑	↑	↑	↑	↑			~	~	↑
Apoptosis		↑	↑	↑/~		↑				↑	~	↑
Metabolic alterations
Glucose oxidation	↓	~		↓				↓	↓/~	↑	↓		↓
FA oxidation	↑	↑	↑	↑	↑		↑	↓	↓	↓	↑		↑
Mitochondrial function	↑	↑	↑				↑	↑		↓		↑	↑
Oxidative stress	↑	↑	↑					↑	↑			↑	↑
Ca2+ mobilization				~	~				↓		~
References	[105, 106]	[107, 108]	[109, 110]	[111, 112]	[113, 114]	[96]	[117, 118]	[103, 104]	[97–99]	[115, 116]	[100]	[101]	[102]

Genetic overexpression of PPARα, PPARγ, long-chain acyl-CoA synthetase-1 (LCACS1), lipoprotein lipase (LPL), fatty acid transport protein-1 (FATP1), PKCβ and uncoupling protein-diphtheria toxin A (UCPDTA), or ablation of cardiac-specific insulin receptor (CIRKO), GLUT4, adipose triglyceride lipase (ATGL), phosphoinositide dependent kinase-1 (PDK1), phosphoinositide-3 kinase (PI3K), and glucokinase (GCK) were forced in rodents for DCM. The associated cardiac effects and the levels of natriuretic peptides in plasma are also highlighted for each model. ↑, ↓ and ~ stand for increased, decreased, or not modified effect, respectively.