Evidence map›Paper›PMID 25862247›Full record

ArticleBiology open2015

Actin-dependent mitochondrial internalization in cardiomyocytes: evidence for rescue of mitochondrial function.

Christina A Pacak, Janine M Preble, Hiroshi Kondo, Peter Seibel, Sidney Levitsky, Pedro J Del Nido, Douglas B Cowan, James D McCully

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biology open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 2 pooled it
4.7field-weighted citation impact, top 4% 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

114 citing papers in PubMed, 2 syntheses or guidelines pooled it, 197 citations in OpenAlex.

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54 more citing papers are in PubMed but not listed here.

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

8 authors at 5 institutions in 2 countries.

Christina A PacakDepartment of Pediatrics, University of Florida College of Medicine, Gainesville, FL 32607, USA.
Janine M PrebleDivision of Cardiac Surgery, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
Hiroshi KondoDivision of Cardiac Surgery, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
Peter SeibelUniversitat Leipzig, Molekulare Zelltherapie, Biotechnologisch-Biomedizinisches Zentrum, 04103 Leipzig, Germany.
Sidney LevitskyDivision of Cardiac Surgery, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA Harvard Medical School, Boston, MA 02115, USA.
Pedro J Del NidoHarvard Medical School, Boston, MA 02115, USA Division of Cardiac Surgery, Boston Children's Hospital, Boston, MA 02115, USA.
Douglas B CowanHarvard Medical School, Boston, MA 02115, USA Department of Anesthesiology, Perioperative and Pain Medicine, Boston Children's Hospital, Boston, MA 02115, USA.
James D McCullyDivision of Cardiac Surgery, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA Harvard Medical School, Boston, MA 02115, USA Division of Cardiac Surgery, Boston Children's Hospital, Boston, MA 02115, USA james_mccully@hms.harvard.edu.
Beth Israel Deaconess Medical Center · USHarvard University · USBoston Children's Hospital · USFlorida College · USLeipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously, we have demonstrated that the transplantation of viable, structurally intact, respiration competent mitochondria into the ischemic myocardium during early reperfusion significantly enhanced cardioprotection by decreasing myocellular damage and enhancing functional recovery. Our in vitro and in vivo studies established that autologous mitochondria are internalized into cardiomyocytes following transplantation; however, the mechanism(s) modulating internalization of these organelles were unknown. Here, we show that internalization of mitochondria occurs through actin-dependent endocytosis and rescues cell function by increasing ATP content and oxygen consumption rates. We also show that internalized mitochondria replace depleted mitochondrial (mt)DNA. These results describe the mechanism for internalization of mitochondria within host cells and provide a basis for novel therapeutic interventions allowing for the rescue and replacement of damaged or impaired mitochondria.

Indexed as

CardioprotectionEndocytosisMitochondriaMitochondrial DNATransplantation

Identifiers

PMID25862247
PMCPMC4434813
OpenAlexW2112450095

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.