Title:The Role of Local Angiotensin II/Angiotensin Type 1-receptor Mechanisms in Adipose Tissue Dysfunction to Promote Pancreatic Cancer
Volume: 24
Issue: 12
Author(s): Rozita Khodashahi, Fatemeh Beiraghdar, Gorgon A. Ferns, Kiayash Ashrafzadeh, Mohsen Aliakbarian*Mohammad-Hassan Arjmand*
Affiliation:
- Transplant Research Center, Clinical Research Institute, Mashhad University of Medical Sciences, Mashhad,
Iran
- Surgical Oncology
Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
- Transplant Research Center, Clinical Research Institute, Mashhad University of Medical Sciences, Mashhad,
Iran
Keywords:
Adipose tissue, obesity, angiotensin II, angiotensin receptor, pancreatic cancer, angiotensin receptor.
Abstract: Obesity and adipose tissue dysfunction are important risk factors for pancreatic cancer.
Pancreatic cancer is one of the most lethal cancers globally. The renin-angiotensin system (RAS)
is expressed in many tissues, including adipose tissue. Dysregulation of angiotensin II and angiotensin
II receptors in adipose tissue through the activation of different signaling pathways leads
to adipose tissue dysfunction, including insulin resistance, adipose tissue inflammation, adipocytokines
secretion, and metabolic alterations. The pathogenesis of pancreatic cancer remains uncertain.
However, there is evidence that dysregulation of local angiotensin II in adipose tissue that occurs
in association with obesity is, in part, responsible for the initiation and progression of pancreatic
cancer. Due to the role of local angiotensin II in the dysfunction of adipose tissue, angiotensin
receptor blockers may be considered a new therapeutic strategy in the amelioration of the complications
related to adipose tissue dysfunction and prevention of pancreatic cancer. This review
aims to consider the biological roles of local angiotensin II and angiotensin II receptors in adipose
tissue dysfunction to promote pancreatic cancer progression with a focus on adipose tissue inflammation
and metabolic reprogramming.