ReviewPflugers Archiv : European journal of physiology2012
Mitochondria and chromaffin cell function.
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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
- Lessons from In Utero and Postnatal Exposure to Pesticide DDT: Mechanisms of Chromaffin Cell Vulnerability and Altered Catecholamine Homeostasis.International journal of molecular sciences · 2026Review
- Histopathological, Biochemical and Molecular Investigations on the Potential Endocrine Disruption of Polystyrene Nanoparticles in Adult Male Albino Rats.Environmental toxicology · 2026Article
- Forty years of the adrenal chromaffin cell through ISCCB meetings around the world.Pflugers Archiv : European journal of physiology · 2023Review
- Mechanisms of Suppression of Epinephrine Production in Rats by Low-Dose Developmental Exposure to DDT.Bulletin of experimental biology and medicine · 2022Article
- Impact of Prenatal and Postnatal Exposure to Endocrine Disrupter DDT on Adrenal Medulla Function.International journal of molecular sciences · 2022Article
- Novel Purine Derivative ITH15004 Facilitates Exocytosis through a Mitochondrial Calcium-Mediated Mechanism.International journal of molecular sciences · 2021Article
- Dichlorodiphenyltrichloroethane and the Adrenal Gland: From Toxicity to Endocrine Disruption.Toxics · 2021Review
- Acute reversible SERCA blockade facilitates or blocks exocytosis, respectively in mouse or bovine chromaffin cells.Pflugers Archiv : European journal of physiology · 2021Article
- Hydrogen sulphide facilitates exocytosis by regulating the handling of intracellular calcium by chromaffin cells.Pflugers Archiv : European journal of physiology · 2018Article
- How does the stimulus define exocytosis in adrenal chromaffin cells?Pflugers Archiv : European journal of physiology · 2018Review
- The Differential Organization of F-Actin Alters the Distribution of Organelles in Cultured When Compared to Native Chromaffin Cells.Frontiers in cellular neuroscience · 2017Article
- The coupling of plasma membrane calcium entry to calcium uptake by endoplasmic reticulum and mitochondria.The Journal of physiology · 2014Review
- Novel features on the regulation by mitochondria of calcium and secretion transients in chromaffin cells challenged with acetylcholine at 37°C.Physiological reports · 2013Article
- A Special Issue on the cell-specific roles of mitochondrial Ca²⁺ handling.Pflugers Archiv : European journal of physiology · 2012Article
- Specific mitochondrial functions in separate sub-cellular domains of pancreatic acinar cells.Pflugers Archiv : European journal of physiology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromaffin cells are an excellent model for stimulus-secretion coupling. Ca(2+) entry through plasma membrane voltage-operated Ca(2+) channels (VOCC) is the trigger for secretion, but the intracellular organelles contribute subtle nuances to the Ca(2+) signal. The endoplasmic reticulum amplifies the cytosolic Ca(2+) ([Ca(2+)](C)) signal by Ca(2+)-induced Ca(2+) release (CICR) and helps generation of microdomains with high [Ca(2+)](C) (HCMD) at the subplasmalemmal region. These HCMD induce exocytosis of the docked secretory vesicles. Mitochondria close to VOCC take up large amounts of Ca(2+) from HCMD and stop progression of the Ca(2+) wave towards the cell core. On the other hand, the increase of [Ca(2+)] at the mitochondrial matrix stimulates respiration and tunes energy production to the increased needs of the exocytic activity. At the end of stimulation, [Ca(2+)](C) decreases rapidly and mitochondria release the Ca(2+) accumulated in the matrix through the Na(+)/Ca(2+) exchanger. VOCC, CICR sites and nearby mitochondria form functional triads that co-localize at the subplasmalemmal area, where secretory vesicles wait ready for exocytosis. These triads optimize stimulus-secretion coupling while avoiding propagation of the Ca(2+) signal to the cell core. Perturbation of their functioning in neurons may contribute to the genesis of excitotoxicity, ageing mental retardation and/or neurodegenerative disorders.
Indexed as
Identifiers
22278417What 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.