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Updated: Jun 5, 2026

Single-cell Transcriptomic Analyses of Mouse Pancreatic Endocrine Cells
Published on: September 30, 2018
Transcriptomic regulation of pancreatic acinar cell homeostasis and plasticity
Xin Zhang1,2, Christopher Luo1,3, Kevin Coughlin1
1Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, NY 11794, U.S.A.
Abstract:
Pancreatic acinar cells are highly specialized secretory epithelial cells in which coordinated transcriptional, epigenetic, and post-transcriptional regulatory mechanisms maintain digestive enzyme production, polarized architecture, and lineage fidelity. This homeostatic network preserves acinar identity while enabling rapid adaptation to physiological stress. Disruption of these regulatory mechanisms triggers acinar-to-ductal metaplasia (ADM), a reversible reprogramming state that supports acinar cell survival and regeneration after acute injury. However, if ADM persists under chronic inflammation or oncogenic KRAS activation, it can facilitate the initiation of pancreatic ductal adenocarcinoma. Elucidating these mechanisms offers opportunities to restore acinar cell homeostasis, reverse ADM, and prevent neoplastic transformation. In this review, we summarize current knowledge on the transcriptional, epigenetic, and post-transcriptional regulation of acinar cell homeostasis and plasticity, with emphasis on their roles in ADM.
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