Evidence map›Paper›PMID 26941425›Full record

ReviewCirculation research2016

Moving Forwards by Blocking Back-Flow: The Yin and Yang of MI Therapy.

Victoria R Pell, Edward T Chouchani, Michael P Murphy, Paul S Brookes, Thomas Krieg

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
9.3field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 102 citations in OpenAlex.

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  19. Key hepatoprotective roles of mitochondria in liver regeneration.American journal of physiology. Gastrointestinal and liver physiology · 2023
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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

5 authors at 2 institutions in 2 countries.

Victoria R PellFrom the Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom (V.R.P., T.K.); Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA (E.T.C.); Department of Cell Biology, Harvard Medical School, Boston, MA (E.T.C.); MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (M.P.M.); and Department of Anesthesiology, University of Rochester Medical Center, Rochester, NY (P.S.B.).
Edward T ChouchaniFrom the Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom (V.R.P., T.K.); Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA (E.T.C.); Department of Cell Biology, Harvard Medical School, Boston, MA (E.T.C.); MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (M.P.M.); and Department of Anesthesiology, University of Rochester Medical Center, Rochester, NY (P.S.B.).
Michael P MurphyFrom the Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom (V.R.P., T.K.); Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA (E.T.C.); Department of Cell Biology, Harvard Medical School, Boston, MA (E.T.C.); MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (M.P.M.); and Department of Anesthesiology, University of Rochester Medical Center, Rochester, NY (P.S.B.).
Paul S BrookesFrom the Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom (V.R.P., T.K.); Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA (E.T.C.); Department of Cell Biology, Harvard Medical School, Boston, MA (E.T.C.); MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (M.P.M.); and Department of Anesthesiology, University of Rochester Medical Center, Rochester, NY (P.S.B.).
Thomas KriegFrom the Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom (V.R.P., T.K.); Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA (E.T.C.); Department of Cell Biology, Harvard Medical School, Boston, MA (E.T.C.); MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (M.P.M.); and Department of Anesthesiology, University of Rochester Medical Center, Rochester, NY (P.S.B.). tk382@medschl.cam.ac.uk.
MRC Mitochondrial Biology Unit · GBHarvard University · US

Funding

SIRT1, Nitro-Lipids and CardioprotectionR01HL071158 · NHLBI · UNIVERSITY OF ROCHESTER · PI BROOKES, PAUL S · 2003 to 2025
$7.7M
British Heart Foundation PG/12/42/29655Medical Research Council MC_U105663142NHLBI NIH HHS R01 HL071158
6 · The paper itself

Abstract

Mitochondrial reactive oxygen species production has emerged as an important pathological mechanism in myocardial ischemia/reperfusion injury. Attempts at targeting reactive oxygen species by scavenging using antioxidants have, however, been clinically disappointing. This review will provide an overview of the current understanding of mitochondrial reactive oxygen species in ischemia/reperfusion injury. We will outline novel therapeutic approaches designed to directly target the mitochondrial respiratory chain and prevent excessive reactive oxygen species production and its associated pathology. This approach could lead to more effective interventions in an area where there is an urgent need for new treatments.

Indexed as

AnimalsCardiovascular AgentsDrug Delivery SystemsHumansMyocardial InfarctionMyocardial Reperfusion InjuryReactive Oxygen SpeciesCardiovascular AgentsReactive Oxygen Speciesantioxidantsmitochondriaoxygenreactive oxygen speciesreperfusion injury

Identifiers

PMID26941425
PMCPMC4809200
OpenAlexW2290552133

What OpenQuestion holds

Textmetadata
LicenceTDM
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.