Pituitary adenylate cyclase-activating polypeptide
Pituitary adenylate cyclase-activating polypeptide has been studied in 1 paper since 2025: none in people yet, 1 in cells. No study of it in people or animals has been published yet. The newest paper, Aug 8, 2025: “PACAP Inhibits TNF-α- Induced Senescence in Primary Chondrocytes by SIRT3: An Implication in Osteoarthritis”.
- 1 lab in 1 country
- Cells1
What did studies of Pituitary adenylate cyclase-activating polypeptide find?
3Studies of Pituitary adenylate cyclase-activating polypeptide measured 3 outcomes; the most studied are SIRT3 (1 study), oxidative stress and ROS signaling (1) and cellular senescence (1).
SIRT3
upin human cells1
1 study
SIRT3
upin human cells1
Pituitary adenylate cyclase-activating polypeptide increases SIRT3 in human cells.
“Mechanistically, PACAP38 upregulated sirtuin 3 (SIRT3), a mitochondrial deacetylase that regulates oxidative stress and metabolism”
Cellsin TNF-α-treated chondrocytes
Clinical and experimental pharmacology & physiology
Oxidative stress and ROS signaling
downin human cells1
1 study
Oxidative stress and ROS signaling
downin human cells1
Pituitary adenylate cyclase-activating polypeptide decreases oxidative stress and ROS signaling in human cells.
“PACAP38 treatment significantly reduced ROS and 8-OHdG levels, restored telomerase activity and telomere length, and decreased SA-β-Gal activity.”
Cellsin TNF-α-treated chondrocytes
Clinical and experimental pharmacology & physiology
Cellular senescence
downin human cells1
1 study
Cellular senescence
downin human cells1
Pituitary adenylate cyclase-activating polypeptide inhibits cellular senescence in human cells.
“PACAP38 treatment significantly reduced ROS and 8-OHdG levels, restored telomerase activity and telomere length, and decreased SA-β-Gal activity.”
Cellsin TNF-α-treated chondrocytes
Clinical and experimental pharmacology & physiology