Anti-VEGF(vascular endothelial growth factor)

Now my question is about pathogenesis of preeclampsia, where in due to underdeveloped placental spiral arteries, they become high resistance, low perfusion vessels.

So, by understanding of simple cardio-physiology, we can understand that if more parallel circuit of arteries was developed, it would have been lower resistance and hence better perfusion, and would not lead to Hypertension and other manifestations of preeclampsia.

Now, everywhere it is mentioned that anti-VEGF is increased in preeclampsia(as it is secreted by the placenta in response to chronic placental ischemia. Now why is placenta secreting anti-VEGF? it doesn't make any sense in decreasing the vessel growth, won't that further worsen the condition? why?

Sources that tell about the anti-VEGF in preeclampsia,

The use of anti-VEGF drugs during pregnancy is controversial because they may potentially cause systemic side effects in the mother and fetal harm, as spontaneous miscarriage and preeclampsia.

(Journal of Ocular Pharmacology and Therapeutics)

Balance of VEGF and anti angiogenic factors

(topic from my text Obstetrics by DC Dutta 8ed Pg257)

Tried searching net but didn't find any hint :(

  • Can you cite sources claiming anti-VEGF is secreted by placenta during preeclampsia? – D.Tan Aug 20 '20 at 23:29

Preeclampsia has to be thought as imbalance in of vascular factors (a theory) Correct way of thinking about Anti VEGF is thinking

  • Anti VEGF are secreted by placenta (for unknown reasons),
  • Decreased synthesis of PgI2 (vasodilator) and
  • increased synthesis of TxA2 (vasoconstrictor) from vascular endothelium,
  • increased sensitivity to Angiotensin II (pressor agent),
  • NO decrease(vasodilator, decreases Plt aggregation, prevent intervillous thrombus)
  • Endothelin -1 (vasoconstrictor)
  • Inflammatory Cytokines (IL-6, TNF alpha)
  • Imbalance of angiogenic and antiangiogenic proteins in placental vascular bed—there is overproduction of two antiangiogenic factors from the trophoblastic tissue. These two antiangiogenic factors are: (a) soluble fms-like tyrosine kinase I (SFlt-1) and (b) soluble endoglin. SFlt-1 binds with VEGF and placental-like growth factor (PLGF) and causes endothelial cell dysfunction

The balance of all these factors appears to be disturbed in preeclampsia, of which anti-VEGF is part off. Which means it might actually be responsible for preeclamsia (or rather we should say it is associated with) and not to be thought as single factor which is released in response to placental ischemia, it is one of multitude of factors responsible/associated with pathogenesis of preeclampsia.

Source: DC Dutta textbook of Obstetrics, 8th ed. Pg 257

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