Evidence map›Paper›PMID 23897815›Full record

ArticleThe Journal of biological chemistry2013

Mitochondria and AMP-activated protein kinase-dependent mechanism of efferocytosis.

Shaoning Jiang, Dae Won Park, William S Stigler, Judy Creighton, Saranya Ravi, Victor Darley-Usmar, Jaroslaw W Zmijewski

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 68 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Beyond Killing: The Overlooked Contribution of Neutrophils to Tissue Repair.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Metabolic Implications of Efferocytosis During Inflammation.Advances in experimental medicine and biology · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Antipsychotic drugs counteract autophagy and mitophagy in multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Review
  20. 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

7 authors at 2 institutions in 2 countries.

Shaoning JiangFrom the Department of Medicine.
Dae Won ParkFrom the Department of Medicine,; the Division of Infectious Diseases, Korea University Ansan Hospital, Ansan 425-707, Republic of Korea.
William S StiglerFrom the Department of Medicine.
Judy CreightonDepartment of Anesthesiology.
Saranya RaviDepartment of Pathology, and.
Victor Darley-UsmarDepartment of Pathology, and; Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0012 and.
Jaroslaw W ZmijewskiFrom the Department of Medicine,; Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0012 and. Electronic address: zmijewsk@uab.edu.
University of Alabama at Birmingham · USAnsan University · KR

Funding

ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
AMPK activates calcium signaling necessary for endothelial barrier repairR01HL102296 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CREIGHTON, JUDY · 2010 to 2014
$1.4M
AMPK activation and acute lung injuryR01HL107585 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZMIJEWSKI, JAROSLAW WALDEMAR · 2012 to 2015
$1.4M
HMGB1 and neutrophil efferocytosis.R01GM087748 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZMIJEWSKI, JAROSLAW WALDEMAR · 2009 to 2012
$1.2M
Impaired AMPK activity contributes to vascular pathogenesis associated with PHR03HL110803 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CREIGHTON, JUDY · 2012 to 2013
$143k
NHLBI NIH HHS HL107585NHLBI NIH HHS R01 HL102296NHLBI NIH HHS R01 HL107585NHLBI NIH HHS R03 HL110803NIAMS NIH HHS P30 AR048311NIAMS NIH HHS P30 AR 48311NIGMS NIH HHS GM87748NIGMS NIH HHS R01 GM087748
6 · The paper itself

Abstract

Defective clearance of apoptotic cells is frequently associated with perpetuation of inflammatory conditions. Our results show a rapid activation of AMP-activated kinase (AMPK) in macrophages upon exposure to apoptotic cells or lysophosphatidylcholine, a specific phospholipid that is produced and released from dying cells. AMPK activation resulted from inhibition of mitochondrial oxygen consumption and ATP production and further depended on Ca(2+) mobilization and mitochondrial reactive oxygen species generation. Once activated, AMPK increased microtubule synthesis and chemokinesis and provided adaptation to energy demand during tracking and engulfment. Uptake of apoptotic cells was increased in lungs of mice that received lysophosphatidylcholine. Furthermore, inhibition of AMPK diminished clearance of apoptotic thymocytes in vitro and in dexamethasone-treated mice. Taken together, we conclude that the mitochondrial AMPK axis is a sensor and enhancer of tracking and removal of apoptotic cell, processes crucial to resolution of inflammatory conditions and a return to tissue homeostasis.

Indexed as

Adenosine TriphosphateAMP-Activated Protein KinasesAnimalsApoptosisCell MovementEnzyme ActivationLungLysophosphatidylcholinesMacrophages, PeritonealMaleMiceMitochondriaOxygen ConsumptionThymocytesAdenosine TriphosphateAMP-Activated Protein KinasesLysophosphatidylcholinesAMP-activated Kinase (AMPK)BioenergeticsChemotaxisMitochondriaPhagocytosis

Identifiers

PMID23897815
PMCPMC3764806
OpenAlexW1977056770

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.