ArticleResearch square2025
Molecular requirements for mammalian crinophagy highlight a key role for Ca
Article in Research square, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Crinophagy in Pancreatic Beta Cells: From Insulin Granule Turnover to Diabetes Pathogenesis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Secretory granules (SGs) in endocrine cells store and release peptide hormones with their turnover tightly controlled to maintain cellular hormone levels. We found that crinophagy, a specialized autophagy process, is the prevalent pathway that degrades older unused SGs in resting cells by SG-lysosome fusion. siRNA screening with a live cell assay for SG-lysosome merge identified SG components Rab27A, Munc13-4 and VAMP2 and lysosomal components PLEKHM1, HOPS subunits, and SNAREs STX7, STX8, and VTI1B required for docking SGs to and fusion with lysosomes. Munc13-4 is a central regulator of crinophagy that associates with many proteins that are functionally essential for the merge of SGs with lysosomes, and regulates the docking and fusion of SGs with lysosomes. SG-lysosome fusion was regulated by local or global calcium through binding and activation of Munc13-4. The findings reveal the critical docking/fusion machinery for mediating SG turnover in mammalian endocrine cells, and indicate how its dysregulation could impair hormonal and metabolic regulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.