Evidence map›Paper›PMID 38632223›Full record

ArticleCell death discovery2024

PGC-1a mediated mitochondrial biogenesis promotes recovery and survival of neuronal cells from cellular degeneration.

Wenting You, Kèvin Knoops, Tos T J M Berendschot, Birke J Benedikter, Carroll A B Webers, Chris P M Reutelingsperger, Theo G M F Gorgels

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
10.3field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 44 citations in OpenAlex.

  1. Norepinephrine regulates hippocampal mitochondrial biogenesis via β2-adrenergic receptor signaling and PGC-1α.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  5. Comparative Study of Young and MaturePlants (Basel, Switzerland) · 2026
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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

7 authors at 2 institutions in 1 country.

Wenting YouUniversity Eye Clinic Maastricht UMC+, Maastricht University Medical Center+, Maastricht, The Netherlands.ORCID http://orcid.org/0000-0002-3954-3219
Kèvin KnoopsThe Microscopy CORE lab, Maastricht Multimodal Molecular Imaging Institute, Maastricht University, Maastricht, The Netherlands.
Tos T J M BerendschotUniversity Eye Clinic Maastricht UMC+, Maastricht University Medical Center+, Maastricht, The Netherlands.
Birke J BenedikterUniversity Eye Clinic Maastricht UMC+, Maastricht University Medical Center+, Maastricht, The Netherlands.
Carroll A B WebersUniversity Eye Clinic Maastricht UMC+, Maastricht University Medical Center+, Maastricht, The Netherlands.
Chris P M ReutelingspergerDepartment of Biochemistry, CARIM School for Cardiovascular Disease, Maastricht University, Maastricht, The Netherlands. c.reutelingsperger@maastrichtuniversity.nl.ORCID http://orcid.org/0000-0002-2334-9403
Theo G M F GorgelsUniversity Eye Clinic Maastricht UMC+, Maastricht University Medical Center+, Maastricht, The Netherlands. theo.gorgels@mumc.nl.ORCID http://orcid.org/0000-0003-0419-2030
Maastricht University Medical Centre · NLMaastricht University · NL

Funding

China Scholarship Council (CSC) 201809110169ZonMw (Netherlands Organisation for Health Research and Development) 435005020
6 · The paper itself

Abstract

Neurodegenerative disorders are characterized by the progressive loss of structure and function of neurons, often including the death of the neuron. Previously, we reported that, by removing the cell death stimulus, dying/injured neurons could survive and recover from the process of regulated cell death, even if the cells already displayed various signs of cellular damage. Now we investigated the role of mitochondrial dynamics (fission/fusion, biogenesis, mitophagy) in both degeneration and in recovery of neuronal cells. In neuronal PC12 cells, exposure to ethanol (EtOH) induced massive neurite loss along with widespread mitochondrial fragmentation, mitochondrial membrane potential loss, reduced ATP production, and decreased total mitochondrial volume. By removing EtOH timely all these mitochondrial parameters recovered to normal levels. Meanwhile, cells regrew neurites and survived. Study of the mitochondrial dynamics showed that autophagy was activated only during the cellular degeneration phase (EtOH treatment) but not in the recovery phase (EtOH removed), and it was not dependent on the Parkin/PINK1 mediated mitophagy pathway. Protein expression of key regulators of mitochondrial fission, phospho-Drp1

Identifiers

PMID38632223
PMCPMC11024166
OpenAlexW4394874936

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.