Table 4.

Gene involvement in preeclampsia and PPCM.

	Role in preeclampsia and PPCM	Ref.
CD274 (PD-L1)	PD-L1 regulates the immune system and is linked to severe inflammation in preeclampsia. More PD-L1 can impair blood vessel function and damage the placenta. The precise relationship between PD-L1 and PPCM is uncertain. However, it may influence how the immune system responds and raises stress levels in the body during PPCM.	[74–77]
FLT1 (Fms-related tyrosine kinase 1)	FLT1 is a VEGF and PlGF receptor. In preeclampsia, elevated levels of sFlt1 have been identified, which bind VEGF and PlGF, limiting their bioavailability and inducing endothelial dysfunction. FLT1 may be involved in PPCM via angiogenesis and vascular homeostasis pathways. Disruptions in these pathways have been linked to cardiovascular dysfunction.	[78–80]
GNB3 (Guanine nucleotide-binding protein subunit beta-3)	GNB3 is a signaling transduction protein that has been linked to blood pressure regulation. GNB3 mutations or polymorphisms may raise the risk of preeclampsia. GNB3's relevance in PPCM is unknown, but given its role in cardiovascular function, changes in this gene may alter the risk or progression of PPCM.	[81–83]
MIR146A	miR-146a is a microRNA that regulates inflammatory responses as well as oxidative stress. miR-146a expression has been altered in preeclampsia, indicating a role in the disease's pathophysiology. miR-146a's effects on inflammatory responses and cellular homeostasis may play a role in PPCM. Changes in miR-146a expression or activity may contribute to cardiac dysfunction.	[84–87]
PDCD1 (PD-1)	PD-1 is an immune checkpoint that controls immune tolerance and protects against autoimmunity. In preeclampsia, disruptions in the PD-1 pathway may contribute to inappropriate immune responses and inflammation. PD-1, like PD-L1, may play a role in modifying immunological responses in PPCM. PD-1 expression or signaling dysregulation could influence the onset and severity of PPCM.	[88–90]
PlGF (placental growth factor)	PlGF levels are frequently reduced in preeclampsia, leading to placental and endothelial dysfunction. PlGF's role in PPCM is unknown, but abnormalities in angiogenesis and tissue perfusion associated with low PlGF levels may contribute to PPCM pathophysiology.	[91–94]
SERPINE1 (serpin family E member 1)	SERPINE1 encodes the PAI-1 inhibitor, which controls fibrinolysis. SERPINE1 expression is increased in preeclampsia, which contributes to thrombosis and vascular dysfunction. Although there is no direct link between SERPINE1 and PPCM, its role in coagulation and vascular homeostasis may impact pathological processes in heart diseases.	[95–99]
VEGFA (vascular endothelial growth factor A)	VEGFA is an important angiogenesis mediator. Endothelial dysfunction, hypertension, and proteinuria can all result from VEGFA pathway malfunction in pregnancy. VEGFA may contribute to the pathogenic mechanisms of PPCM, such as endothelial dysfunction and cardiac remodeling, through its role in angiogenesis and vascular integrity.	[100–102]