Evidence map›Paper›PMID 39378840›Full record

ReviewDevelopmental cell2024

Dynamic death decisions: How mitochondrial dynamics shape cellular commitment to apoptosis and ferroptosis.

Jesminara Khatun, Jesse D Gelles, Jerry Edward Chipuk

Abstract readReview
In one paragraph

Review in Developmental cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed.

  1. Article
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  4. Review
  5. Article
  6. Molecularly Engineered Phenoxazinone-Skeleton Cascade-Activated NIR Probes for Monitoring FeAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  8. Article
  9. Review
  10. Article
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  12. Review
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  14. Review
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  16. Review
  17. Review
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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

3 authors.

Jesminara KhatunDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Jesse D GellesDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Jerry Edward ChipukDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; Department of Dermatology, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; The Diabetes, Obesity, and Metabolism Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA. Electronic address: jerry.chipuk@mssm.edu.

Funding

THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Ramon E Parsons · 2015 to 2026
$35.4M
Chronic Mitochondrial Division and Melanoma: Mechanism, Prognosis, and TherapyR01CA267696 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Jerry Edward Chipuk · 2022 to 2026
$2.4M
The Oncogene Activated Mitochondrial Unfolded Protein Response Regulates Senescence BiologyR01CA271346 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Jerry Edward Chipuk · 2023 to 2026
$2.4M
Function and Regulation of the BCL-2 FamilyR01CA237264 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHIPUK, JERRY EDWARD · 2020 to 2024
$1.9M
NCI NIH HHS P30 CA196521NCI NIH HHS R01 CA237264NCI NIH HHS R01 CA267696NCI NIH HHS R01 CA271346
6 · The paper itself

Abstract

The incorporation of mitochondria into early eukaryotes established organelle-based biochemistry and enabled metazoan development. Diverse mitochondrial biochemistry is essential for life, and its homeostatic control via mitochondrial dynamics supports organelle quality and function. Mitochondrial crosstalk with numerous regulated cell death (RCD) pathways controls the decision to die. In this review, we will focus on apoptosis and ferroptosis, two distinct forms of RCD that utilize divergent signaling to kill a targeted cell. We will highlight how proteins and processes involved in mitochondrial dynamics maintain biochemically diverse subcellular compartments to support apoptosis and ferroptosis machinery, as well as unite disparate RCD pathways through dual control of organelle biochemistry and the decision to die.

Indexed as

ApoptosisFerroptosisMitochondriaMitochondrial DynamicsAnimalsHumansSignal Transductionapoptosiscell biologycell deathferroptosismembranesmitochondriamitochondrial dynamicssignal transduction

Identifiers

PMID39378840
PMCPMC11469553

What OpenQuestion holds

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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.