ReviewPflugers Archiv : European journal of physiology2012
Specific mitochondrial functions in separate sub-cellular domains of pancreatic acinar cells.
Review in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
15 citing papers in PubMed, 26 citations in OpenAlex.
- Tangled contacts: mitochondrial interactions with cellular organelles in acute pancreatitis.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- Mitochondrial dysfunction as a bridge to pathology in acute pancreatitis: From molecular insights to novel therapeutic strategies.World journal of gastroenterology · 2025Review
- Mitochondrial dysfunction in pancreatic acinar cells: mechanisms and therapeutic strategies in acute pancreatitis.Frontiers in immunology · 2024Review
- Review
- Review
- CaCold Spring Harbor perspectives in biology · 2020Review
- CRAC channels in secretory epithelial cell function and disease.Cell calcium · 2019Review
- Basal Mitophagy Occurs Independently of PINK1 in Mouse Tissues of High Metabolic Demand.Cell metabolism · 2018Article
- NeuCode Proteomics Reveals Bap1 Regulation of Metabolism.Cell reports · 2016Article
- Genetic inhibition of protein kinase Cε attenuates necrosis in experimental pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- The coupling of plasma membrane calcium entry to calcium uptake by endoplasmic reticulum and mitochondria.The Journal of physiology · 2014Review
- Ca2+ release-activated Ca2+ channel blockade as a potential tool in antipancreatitis therapy.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Mitochondrial Ca²⁺ homeostasis: mechanism, role, and tissue specificities.Pflugers Archiv : European journal of physiology · 2012Review
- Mitochondrial function and malfunction in the pathophysiology of pancreatitis.Pflugers Archiv : European journal of physiology · 2012Review
- A Special Issue on the cell-specific roles of mitochondrial Ca²⁺ handling.Pflugers Archiv : European journal of physiology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The pancreatic acinar cell synthesizes many digestive proenzymes, which are packaged into secretory (zymogen) granules and secreted by exocytosis upon the action of the neurotransmitter acetylcholine, released from vagal nerve endings, or the hormone cholecystokinin. These secretagogues mobilize Ca(2+) from internal stores and thereby create the cytosolic Ca(2+) signals that control exocytosis. Exocytosis requires Ca(2+), Mg(2+) and ATP. Mg(2+) is present in millimolars concentration throughout the cytosol, but high cytosolic Ca(2+) concentrations need to be created in the local domains near the apical plasma membrane. A special group of mitochondria surrounding the apical granular area play a crucial role in confining cytosolic Ca(2+) elevations to this part of the cell by acting as a Ca(2+) buffer barrier. The Ca(2+) uptake into these mitochondria during apical Ca(2+) spiking stimulates mitochondrial ATP synthesis. ATP is also required for Ca(2+) extrusion via the plasma membrane Ca(2+) pumps, mainly located in the apical area, as well as for Ca(2+) reuptake into the endoplasmic reticulum. Because Ca(2+) extrusion occurs during Ca(2+) spiking, there is a need for compensatory Ca(2+) entry via store-operated Ca(2+) channels. Sub-plasmalemmal (peripheral) mitochondria play an important role in supporting both store-operated Ca(2+) entry at the base as well as the subsequent Ca(2+) pumping into the endoplasmic reticulum. A third group of mitochondria surround the nucleus. They protect the nucleus against unwarranted Ca(2+) signals generated elsewhere and are capable of confining Ca(2+) signals primarily generated inside the nucleus to this part of the cell.
Indexed as
Identifiers
What OpenQuestion holds
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.