Key Study: Activin A Follistatin Like 3

Ansh Labs' Activin A and Follistatin Like-3 ELISA kits were used in a ground-breaking study on preeclampsia and peripartum cardiomyopathy.

Placental senescence pathophysiology is shared between peripartum cardiomyopathy and preeclampsia in mouse and human.

https://www.science.org/doi/10.1126/scitranslmed.adi0077

Cardiovascular diseases are a leading cause of maternal death worldwide. Peripartum cardiomyopathy (PPCM), an idiopathic form of acute systolic heart failure (HF) that occurs during late pregnancy or early postpartum, is a major cause of maternal mortality. The incidence of PPCM is around 1 in 1000 in the United States, but as high as I in 1 in 100 in Nigeria, and is rising because of increasing prevalence of its risk factors, which include preeclampsia, advanced maternal age, and multiple gestation pregnancies.

Among the 28 shared SASP proteins, activin A was the most highly up-regulated in preeclamptic placenta (gene ID: INHBA, 5.0 fold, P = 0.0008). Moreover, established downstream targets of activin A signaling, including follistatin-like 3 (FSTL3) and serpin family E member 1 (SERPINEl), were the next two most highly upregulated SASP genes, suggesting a role for activin biology in these pregnancy-induced cardiovascular diseases.

In both cohorts, serum activin A concentrations were not only higher in patients with preeclampsia or PPCM, compared with matched pregnant and nonpregnant controls, but also associated with worsening cardiac function and/or HF severity. Evidence of increased activin A signaling was also detected in the hearts of women with advanced PPCM compared with individuals without HF. Moreover, plasma from patients with preeclampsia versus matched normotensive pregnant controls directly induced transcriptional profiles of activin A signaling and non-significantly increased pathologic gene expression profiles (NPPB and MYH7, P = 0.1) in human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs), independent of hemodynamic influences. Together, these data raised the possibility that placental-derived SASP proteins, specifically activin A, could contribute to the development of acute cardiac dysfunction in pregnancy-induced HF syndromes.

Source:

Jason D. Roh et al., Placental senescence pathophysiology is shared between peripartum cardiomyopathy and preeclampsia in mouse and human.Sci. Transl. Med.16, eadi0077(2024). Available at: https://www.science.org/doi/10.1126/scitranslmed.adi0077

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NOTE: Activin A and Follistatin Like-3 are for Research Use Only.

#preeclampsia #peripartumcardiomyopathy #activina #follistatinlike-3 #ELISA #immunoassay

All information is provided for educational purposes. All assays indicated are for Research Use Only