Pancreatic ducts
You want them healthy: they are a regenerative reserve when intact and a fibrotic driver when damaged.
In depth
The cells lining the tubes that carry enzymes out of the pancreas. They are the second place new beta cells can come from — and they are also where fibrosis begins when the tubes are injured. The same cell type sits on both sides of this blend.
What drives it
Coxsackievirus B3 reduces it.
10.1128/msphere.00036-23 — Verbatim, and it contradicts the received view: 'Contrary to prior claims, our analysis reveals no evidence of preferential viral tropism for beta and ductal cells, instead demonstrating comparable infection rates across both endocrine and exocrine compartments. Beta, alpha, and ductal cells show the most robust transcriptional responses to infection, with ductal cells, not beta cells, exhibiting the strongest interferon- and hla-associated responses' (Cell Reports, s2211124725009829, primary human islets, single-cell). This 2025 study disagrees with the beta-cell-tropism literature cited on the CVB3 to beta-cell link. Both sides are shown on purpose. doi 10.1128/msphere.00036-23
What it drives
It increases Beta-cell renewal.
10.1371/journal.pone.0004734 — The second source of new beta cells. Verbatim (CIBERISCIII, Spain): 'han demostrado que las células beta se regeneran desde DOS Fuentes diferentes: a partir de la transformación de las células alfa en beta y también mediante LA FORMACIÓN DE NUEVAS CÉLULAS beta PRODUCTORAS DE Insulina EN LOS DUCTOS PANCREÁTICOS' — beta cells regenerate from two different sources: transformation of alpha cells into beta cells, and the formation of new insulin-producing beta cells in the pancreatic ducts. demonstrated in a type 1 mouse model under LIRAGLUTIDE, a GLP-1 receptor agonist selected by neural-network screening of 6,605 drugs. Nothing on this blend is A GLP-1 agonist at a regenerative dose. This edge explains a route; it does not license a claim. doi 10.1371/journal.pone.0004734
It increases Pancreatic stellate cells.
The same cell, the other direction. Verbatim: 'A vicious profibrotic signaling cycle involving injured ducts, pancreatic stellate cells and macrophages with increased levels of pancreatic tissue TGF-beta at the core has increasingly been recognized as an essential driver of pancreatic exocrine fibrosis' (Diabetologia, doi 10.1007/s00125-026-06678-6). The link runs directly: injured ducts drive stellate activation — the pathway is duct-cell health, so a damaged duct is a low-health duct feeding fibrosis. The review's own verbs are 'potential' and 'we propose'. doi 10.1007/s00125-026-06678-6
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.