Evidence map›Paper›PMID 27798841›Full record

ReviewGenes & development2016

Interrogating the relevance of mitochondrial apoptosis for vertebrate development and postnatal tissue homeostasis.

Selma Tuzlak, Thomas Kaufmann, Andreas Villunger

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  3. International journal of endocrinology · 2026
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  7. Contemporary oncology (Poznan, Poland) · 2025
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  20. Role of Apoptosis in HIV Pathogenesis.Advances in virology · 2022
    Review
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

3 authors at 2 institutions in 2 countries.

Selma TuzlakDivision of Developmental Immunology, Biocenter, Medical University Innsbruck, A6020 Innsbruck, Austria.ORCID 0000-0001-8259-4153
Thomas KaufmannInstitute of Pharmacology, University of Bern, Inselspital, CH3010 Bern, Switzerland.
Andreas VillungerDivision of Developmental Immunology, Biocenter, Medical University Innsbruck, A6020 Innsbruck, Austria.
Innsbruck Medical University · ATUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

"Programmed cell death or 'apoptosis' is critical for organogenesis during embryonic development and tissue homeostasis in the adult. Its deregulation can contribute to a broad range of human pathologies, including neurodegeneration, cancer, or autoimmunity…" These or similar phrases have become generic opening statements in many reviews and textbooks describing the physiological relevance of apoptotic cell death. However, while the role in disease has been documented beyond doubt, facilitating innovative drug discovery, we wonder whether the former is really true. What goes wrong in vertebrate development or in adult tissue when the main route to apoptotic cell death, controlled by the BCL2 family, is impaired? Such scenarios have been mimicked by deletion of one or more prodeath genes within the BCL2 family, and gene targeting studies in mice exploring the consequences have been manifold. Many of these studies were geared toward understanding the role of BCL2 family proteins and mitochondrial apoptosis in disease, whereas fewer focused in detail on their role during normal development or tissue homeostasis, perhaps also due to an irritating lack of phenotype. Looking at these studies, the relevance of classical programmed cell death by apoptosis for development appears rather limited. Together, these many studies suggest either highly selective and context-dependent contributions of mitochondrial apoptosis or significant redundancy with alternative cell death mechanisms, as summarized and discussed here.

Indexed as

AnimalsApoptosisEmbryonic DevelopmentHomeostasisMitochondriaProto-Oncogene Proteins c-bcl-2VertebratesProto-Oncogene Proteins c-bcl-2BCL2 familyBH3-only proteinscell deathdevelopmenttissue homeostasis

Identifiers

PMID27798841
PMCPMC5088563
OpenAlexW2534033388

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.