Evidence map›Paper›PMID 33807810›Full record

ReviewCells2021

Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung Injuries.

Vadim S Ten, Anna A Stepanova, Veniamin Ratner, Maria Neginskaya, Zoya Niatsetskaya, Sergey Sosunov, Anatoly Starkov

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  10. Pharmacological Effect ofBioMed research international · 2022
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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

7 authors at 4 institutions in 1 country.

Vadim S TenDepartments of Pediatrics, Columbia University Irving Medical Center, New York, NY 10032, USA.
Anna A StepanovaDepartments of Pediatrics, Columbia University Irving Medical Center, New York, NY 10032, USA.
Veniamin RatnerDepartment of Pediatrics, Icahn Mount Sinai School of Medicine, New York, NY 10029, USA.
Maria NeginskayaDepartment Molecular Pathobiology, New York University School of Dentistry, New York, NY 10010, USA.
Zoya NiatsetskayaDepartments of Pediatrics, Columbia University Irving Medical Center, New York, NY 10032, USA.
Sergey SosunovDepartments of Pediatrics, Columbia University Irving Medical Center, New York, NY 10032, USA.
Anatoly StarkovNeuroscience Department, Weil-Cornell School of Medicine, New York, NY 10065, USA.
Columbia University Irving Medical Center · USCornell University · USIcahn School of Medicine at Mount Sinai · USNew York University · US

Funding

TRANSCRIPTIONAL RESPONSES TO MITOCHONDRIAL DYSFUNCTIONP01AG014930 · NIA · WINIFRED MASTERSON BURKE MED RES INST · PI GIBSON, GARY E · 1999 to 2020
$30.7M
Mitochondrial complex-I as a target for metabolic resuscitation in perinatal hypoxic-ischemic brain injuryR01NS100850 · NINDS · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI TEN, VADIM S · 2017 to 2021
$2.0M
Mitochondrial Dysfunction and White Matter InjuryR01NS099109 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TEN, VADIM S · 2016 to 2020
$1.8M
NIA NIH HHS P01 AG014930NINDS NIH HHS R01 NS099109NINDS NIH HHS R01 NS100850
6 · The paper itself

Abstract

This review discusses the potential mechanistic role of abnormally elevated mitochondrial proton leak and mitochondrial bioenergetic dysfunction in the pathogenesis of neonatal brain and lung injuries associated with premature birth. Providing supporting evidence, we hypothesized that mitochondrial dysfunction contributes to postnatal alveolar developmental arrest in bronchopulmonary dysplasia (BPD) and cerebral myelination failure in diffuse white matter injury (WMI). This review also analyzes data on mitochondrial dysfunction triggered by activation of mitochondrial permeability transition pore(s) (mPTP) during the evolution of perinatal hypoxic-ischemic encephalopathy. While the still cryptic molecular identity of mPTP continues to be a subject for extensive basic science research efforts, the translational significance of mitochondrial proton leak received less scientific attention, especially in diseases of the developing organs. This review is focused on the potential mechanistic relevance of mPTP and mitochondrial dysfunction to neonatal diseases driven by developmental failure of organ maturation or by acute ischemia-reperfusion insult during development.

Indexed as

Brain InjuriesHumansInfant, NewbornLung InjuryMitochondriaPermeabilitybrainlungsmitochondriaprematurityproton leak

Identifiers

PMID33807810
PMCPMC7999701
OpenAlexW3134865517

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.