JOURNAL ARTICLE
REVIEW
Add like
Add dislike
Add to saved papers

TGF-β in Pancreatic Disease: Mechanisms and Therapeutic Potential.

Pancreatic disease, such as acute pancreatitis (AP), chronic pancreatitis (CP) and pancreatic cancer (PC), is a common gastrointestinal disease resulting in the development of local and systemic complications with a significant risk of death. A host of studies on pancreatic disease have been conducted over the past few decades, however, the pathogenesis remains obscure, and there is still a lack of effective treatment options. Recently, there are emerging evidences that transforming growth factor beta (TGF-β) exerts controversial function in apoptosis, inflammatory response and carcinogenesis, which makes its roles more complex in the pathogenesis of pancreas-associated disease. Therefore, further understanding of relevant TGF-β signaling will provide new idea and potential therapeutic targets that can prevent disease progression. Here, as far as we know, we are the first one to systemically review recent data from animal and human clinical studies that focus on TGF-β signaling in a set of pancreas damage and disease, and the potentially promising development of therapeutic agents to regulate TGF-β on this pathology for preventing or treating pancreatic disease.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app