Table 3.

Summary for the role of TRPV1 channels in HF.

	Treatment to Modulate TRPV1	TRPV1 up- or Downmodulation	Experimental Model	Effect of Treatment on Major Study Endpoints	Role of TRPV1 Activation on Cardiac Remodeling	Reference(s)
Capsaicin-sensitive sensory nerve desensitization	neonatal capsaicin treatment	↓	neonatal capsaicin treatment, dilated cardiomyopathy (DCM) and control rat	enhanced EPR compared to control	detrimental	[101]
	epicardial TRPV1 ablation by high dose RTX	epicardial ↓	post-MI-induced HF with RTX treatment in rat	improved cardiac compliance	detrimental	[105]
	intrathecal RTX treatment	spinal cord ↓	transverse aortic constriction (TAC)-induced HF	improved cardiac function	detrimental	[106]
	sc. capsaicin treatment for 3 days at increasing doses	↓	sensory neuropathy-induced HFpEF	impaired myocardial relaxation	beneficial	[103,104]
Pharmacological or genetic modulation of the TRPV1 receptor	genetic deletion	↓	7 days post-MI mouse	increased infarct size	beneficial	[108]
	genetic deletion and dietary capsaicin for 24 weeks	↑	high-salt diet-induced cardiac hypertrophy, mouse	improved mitochondrial function	beneficial	[111]
	TRPV1 gene disruption	↓	TAC-induced HF	reduced cardiac hypertrophy	detrimental	[113]
	genetic deletion	↓	TAC-induced HF	decreased cardiac function and increased TNFα and IL-6	beneficial	[112]
	genetic deletion and dietary capsaicin for 10 weeks	↑	TAC-induced HF	attenuated hypertrophy in WT	beneficial	[114]
	TRPV1 activation by eugenol, capsazepine	↑	acute doxorubicin cardiotoxicity	improved cardiac function	beneficial	[117]
	SA13353 TRPV1 agonist, and capsazepine	↑	doxorubicin-induced HF, ALDH2 transgene mouse	improved cardiac function	beneficial	[116]
	genetic deletion, AMG-9810 TRPV1 antagonist	↓	LPS-induced endotoxemia, mouse	cardiac dysfunction	beneficial	[120]