Experimental studies indicated that LDZGD improved myocardial tissue injury and resisted ventricular remodeling by inhibiting the inflammatory response in HF.[15] It also delayed progression of disease by inhibiting the overactivation of renin-angiotensin-aldosterone system in rats of CHF.[16] Network pharmacological study demonstrated that LGZGD improved CHF may be related to the regulation of renin-angiotensin-aldosterone system and sympathetic nervous system.[17]. The gene discussed is REN; the disease is hydrops fetalis.