Evidence map›Paper›PMID 33912918›Full record

ReviewJournal of cell science2021

The role of nuclear Ca2+ in maintaining neuronal homeostasis and brain health.

Pawel Mozolewski, Maciej Jeziorek, Christoph M Schuster, Hilmar Bading, Bess Frost, Radek Dobrowolski

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cell science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.1field-weighted citation impact, top 5% of its field
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

16 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. bioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. CaFrontiers in endocrinology · 2024
    Review
  10. Article
  11. Amyloid β-Oligomers Inhibit the Nuclear CaAntioxidants (Basel, Switzerland) · 2023
    Article
  12. Store-Operated CaJournal of clinical medicine · 2023
    Review
  13. Integration of nuclear CaCellular and molecular life sciences : CMLS · 2023
    Article
  14. Article
  15. Review
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Pawel MozolewskiDepartment of Biological Sciences, Rutgers University, Newark, NJ 07102, USA.
Maciej JeziorekDepartment of Biological Sciences, Rutgers University, Newark, NJ 07102, USA.
Christoph M SchusterDepartment of Neurobiology, Interdisciplinary Center for Neurosciences (IZN), Heidelberg University, INF 345 and INF 366, 69120 Heidelberg, Germany.
Hilmar BadingDepartment of Neurobiology, Interdisciplinary Center for Neurosciences (IZN), Heidelberg University, INF 345 and INF 366, 69120 Heidelberg, Germany.
Bess FrostGlenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, University of Texas Health, San Antonio , San Antonio , TX 78229, USA.
Radek DobrowolskiDepartment of Biological Sciences, Rutgers University, Newark, NJ 07102, USA.
Rutgers, The State University of New Jersey · USHeidelberg University · DEThe University of Texas Health Science Center at San Antonio · US

Funding

Mechanisms of tau- and aging-induced neurological dysfunction: Focus on the nucleusR01AG057896 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FROST, BESS · 2019 to 2023
$2.8M
Regulation of Neuronal Clearance Pathways via Nuclear Calcium Signaling in Alzheimer's DiseaseR01AG062475 · NIA · RUTGERS THE STATE UNIV OF NJ NEWARK · PI FRIEDMAN, WILMA J · 2019 to 2023
$2.3M
Mucolipin-1-Mediated Mechanisms of Neuronal Clearance in Alzheimer’s DiseaseR56AG061040 · NIA · RUTGERS THE STATE UNIV OF NJ NEWARK · PI KIM, HAESUN A · 2019 to 2019
$385k
NIA NIH HHS R01 AG057896NIA NIH HHS R01 AG062475NIA NIH HHS R56 AG061040
6 · The paper itself

Abstract

Nuclear Ca2+ has emerged as one of the most potent mediators of the dialogue between neuronal synapses and the nucleus that regulates heterochromatin states, transcription factor activity, nuclear morphology and neuronal gene expression induced by synaptic activity. Recent studies underline the importance of nuclear Ca2+ signaling in long-lasting, activity-induced adaptation and maintenance of proper brain function. Diverse forms of neuroadaptation require transient nuclear Ca2+ signaling and cyclic AMP-responsive element-binding protein (CREB1, referred to here as CREB) as its prime target, which works as a tunable switch to drive and modulate specific gene expression profiles associated with memory, pain, addiction and neuroprotection. Furthermore, a reduction of nuclear Ca2+ levels has been shown to be neurotoxic and a causal factor driving the progression of neurodegenerative disorders, as well as affecting neuronal autophagy. Because of its central role in the brain, deficits in nuclear Ca2+ signaling may underlie a continuous loss of neuroprotection in the aging brain, contributing to the pathophysiology of Alzheimer's disease. In this Review, we discuss the principles of the 'nuclear calcium hypothesis' in the context of human brain function and its role in controlling diverse forms of neuroadaptation and neuroprotection. Furthermore, we present the most relevant and promising perspectives for future studies.

Indexed as

CalciumNeuronsBrainCyclic AMP Response Element-Binding ProteinHomeostasisHumansSynapsesCalciumCyclic AMP Response Element-Binding ProteinAlzheimer's diseaseAutophagyCREB signalingEpigeneticsLysosomeNuclear calcium

Identifiers

PMID33912918
PMCPMC8084578
OpenAlexW3158570035

What OpenQuestion holds

Textmetadata
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.