Pre-Eclampsia Clinical Trial
Official title:
Diyarbakir Women's and Children's Diseases Hospital
The complement C1q tumor necrosis factor-associated protein-9 (CTRP-9), which is responsible for regulating cardiovascular and metabolic functions, increases vascular relaxation by pathway dependent on AMPK / endothelial nitric oxide synthesis (eNOS). The aim of this study was to investigate CTRP-9 levels in pregnant women with preeclampsia.
The most important reason for the development of preeclampsia is the problem of
trophoblastinvasion and consequent formation and development of placenta is not healthy
Cytokines are regulatory molecules that have effects on cell functions.Cytokines are
molecules that also regulate endothelial functions. Placenta formation and widespread
endothelial damage are under the influence of cytokines.
Therefore, there may be important links between impairment or imbalance in cytokine release
and function and the formation of preeclampsia.Nitric oxide (NO) is a biologic enzyme that is
synthesized by nitric oxide synthase (NOS) from the amino acid of L-arginine and exists in
all mammals.
e(NOS) is the three isoforms of NO. It is known that NO is a major vasodilator of pregnancy,
inhibiting platelet and leukocyte aggregation.There was a decrease in NO levels in
preeclamptic patients.
The CqP / TNF Binding Protein (CTRP) family consists of 15 members, and is synthesized in
many organs outside the body of fat.CTRP9 is predominantly excreted in fat tissue, and levels
in circulation are reduced in patients with diabetes and obesity.Many studies have shown that
CTRP9 exerts beneficial effects on metabolic and cardiovascular homeostasis.
CTRP9 increases vascular relaxation in the AMPK / endothelial nitric oxide synthase (eNOS)
dependent pathway. CTRP9 has also been reported to reduce inflammatory responses in
endothelial cells via the AMPK-dependent pathway.
Vasorelaxation due to CTRP9 is endothelium-dependent and NO-mediated. CTRP9, directly acting
on smooth muscle, is indirectly or indirectly associated with NO production in the vascular
endothelial layer by stimulating vasorelaxial molecular production by endothelial cells.
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