Evidence map›Paper›PMID 27397688›Full record

ArticleMolecular cell2016

Redox Nanodomains Are Induced by and Control Calcium Signaling at the ER-Mitochondrial Interface.

David M Booth, Balázs Enyedi, Miklós Geiszt, Péter Várnai, György Hajnóczky

Abstract read
In one paragraph

Article in Molecular cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers.

0numbers the graph read from it
0cells of the map it votes in
174citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

174 citing papers in PubMed.

  1. A mathematical theory of redox biology.Royal Society open science · 2026
    Article
  2. Review
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  6. Redox signals and oxidative stress in the control of mitochondrial protein import.Protein science : a publication of the Protein Society · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. Peroxisome calcium uptake is dependent on ER-peroxisome membrane contact.Cellular and molecular life sciences : CMLS · 2026
    Article
  11. Article
  12. Article
  13. Review
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114 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

David M BoothMitoCare Center, Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Balázs EnyediDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1444 Budapest, Hungary.
Miklós GeisztDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1444 Budapest, Hungary.
Péter VárnaiDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1444 Budapest, Hungary.
György HajnóczkyMitoCare Center, Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA. Electronic address: gyorgy.hajnoczky@jefferson.edu.

Funding

ZERNIKE PHASE-CONTRAST IMAGINGP41RR001219 · NCRR · WADSWORTH CENTER · PI WAGENKNECHT, TERENCE C · 1985 to 2010
$11.1M
MITOCHONDRIAL CALCIUM SIGNALING IN CELL DEATHR01GM059419 · NIGMS · THOMAS JEFFERSON UNIVERSITY · PI HAJNOCZKY, GYORGY · 2000 to 2016
$4.0M
Study of the mitochondrial-cellular response to environmental stress by flourescence imagingR33ES025672 · NIEHS · THOMAS JEFFERSON UNIVERSITY · PI CSORDAS, GYORGY, HAJNOCZKY, GYORGY · 2017 to 2019
$1.5M
Redox Regulation of Intracellular Calcium SignalingR01DK103558 · NIDDK · THOMAS JEFFERSON UNIVERSITY · PI HAJNOCZKY, GYORGY, JOSEPH, SURESH K · 2015 to 2018
$1.4M
Study of the mitochondrial-cellular response to environmental stress by flourescence imagingR21ES025672 · NIEHS · THOMAS JEFFERSON UNIVERSITY · PI CSORDAS, GYORGY, HAJNOCZKY, GYORGY · 2015 to 2016
$423k
NCRR NIH HHS P41 RR001219NIDDK NIH HHS R01 DK103558NIEHS NIH HHS R21 ES025672NIEHS NIH HHS R33 ES025672NIGMS NIH HHS R01 GM059419
6 · The paper itself

Abstract

The ER-mitochondrial interface is central to calcium signaling, organellar dynamics, and lipid biosynthesis. The ER and mitochondrial membranes also host sources and targets of reactive oxygen species (ROS), but their local dynamics and relevance remained elusive since measurement and perturbation of ROS at the organellar interface has proven difficult. Employing drug-inducible synthetic ER-mitochondrial linkers, we overcame this problem and demonstrate that the ER-mitochondrial interface hosts a nanodomain of H2O2, which is induced by cytoplasmic [Ca(2+)] spikes and exerts a positive feedback on calcium oscillations. H2O2 nanodomains originate from the mitochondrial cristae, which are compressed upon calcium signal propagation to the mitochondria, likely due to Ca(2+)-induced K(+) and concomitant water influx to the matrix. Thus, ER-mitochondrial H2O2 nanodomains represent a component of inter-organelle communication, regulating calcium signaling and mitochondrial activities.

Indexed as

Calcium SignalingCalciumCalcium ChannelsEndoplasmic ReticulumGenes, ReporterHep G2 CellsHumansHydrogen PeroxideMembrane MicrodomainsMicroscopy, FluorescenceMitochondria, LiverMitochondrial MembranesOxidation-ReductionRecombinant Fusion ProteinsTime FactorsTransfectionCalciumCalcium ChannelsHydrogen PeroxideRecombinant Fusion Proteins

Identifiers

PMID27397688
PMCPMC4998968

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.