Evidence map›Paper›PMID 39580803›Full record

ArticleCell reports2024

AMPK regulates Bcl2-L-13-mediated mitophagy induction for cardioprotection.

Tomokazu Murakawa, Jumpei Ito, Mara-Camelia Rusu, Manabu Taneike, Shigemiki Omiya, Javier Moncayo-Arlandi, Chiaki Nakanishi, Ryuta Sugihara, Hiroki Nishida, Kentaro Mine and 7 more

Abstract read
In one paragraph

Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Regulation and roles of mammalian mitophagy.Nature reviews. Molecular cell biology · 2026
    Review
  2. Review
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  4. Mitophagy in cardiovascular diseases: a literature review.Cardiovascular diagnosis and therapy · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Mechanism and regulation of mitophagy in liver diseases: a review.Frontiers in cell and developmental biology · 2025
    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

17 authors.

Tomokazu MurakawaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK.
Jumpei ItoThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK; National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan.
Mara-Camelia RusuThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK.
Manabu TaneikeDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK.
Shigemiki OmiyaThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK; National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan.
Javier Moncayo-ArlandiThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK.
Chiaki NakanishiThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK; National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan.
Ryuta SugiharaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Hiroki NishidaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Kentaro MineDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Roland FleckCentre for Ultrastructural Imaging, New Hunts House, King's College London, SE1 1UL London, UK; Randall Centre for Cell and Molecular Biophysics, King's College London, SE1 1UL London, UK.
Min ZhangThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK.
Kazuhiko NishidaThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK.
Ajay M ShahThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK.
Osamu YamaguchiNational Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan; Department of Cardiology, Pulmonology, Hypertension & Nephrology, Ehime University Graduate School of Medicine, 454 Shitsukawa, Toon, Ehime 791-0295, Japan.
Yasushi SakataDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Kinya OtsuThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, 125 Coldharbour Lane, SE5 9NU London, UK; National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan. Electronic address: otsu.kinya@ncvc.go.jp.

Funding

British Heart Foundation CH/11/3/29051British Heart Foundation RG/16/15/32294
6 · The paper itself

Abstract

The accumulation of damaged mitochondria in the heart is associated with heart failure. Mitophagy is an autophagic degradation system that specifically targets damaged mitochondria. We have reported previously that Bcl2-like protein 13 (Bcl2-L-13) mediates mitophagy and mitochondrial fission in mammalian cells. However, the in vivo function of Bcl2-L-13 remains unclear. Here, we demonstrate that Bcl2-L-13-deficient mice and knockin mice, in which the phosphorylation site (Ser272) on Bcl2-L-13 was changed to Ala, showed left ventricular dysfunction in response to pressure overload. Attenuation of mitochondrial fission and mitophagy led to impairment of ATP production in these mouse hearts. In addition, we identified AMPKα2 as the kinase responsible for the phosphorylation of Bcl2-L-13 at Ser272. These results indicate that Bcl2-L-13 and its phosphorylation play an important role in maintaining cardiac function. Furthermore, the amplitude of stress-stimulated mitophagic activity could be modulated by AMPKα2.

Indexed as

AMP-Activated Protein KinasesMitophagyProto-Oncogene Proteins c-bcl-2Adenosine TriphosphateAnimalsHumansMaleMiceMice, Inbred C57BLMice, KnockoutMitochondrial DynamicsMyocardiumMyocytes, CardiacPhosphorylationAdenosine TriphosphateAMP-Activated Protein KinasesPrkaa2 protein, mouseProto-Oncogene Proteins c-bcl-2Bcl2-L-13CP: Cell biologyheart failuremitochondriamitophagy

Identifiers

PMID39580803
PMCPMC11672683

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Registered trials

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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.