Evidence map›Paper›PMID 32515224›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2020

Metabolic alterations caused by the mutation and overexpression of the

Wei-Hua Lee, Vijesh J Bhute, Hitoshi Higuchi, Sakae Ikeda, Sean P Palecek, Akihiro Ikeda

Open access · bronzeAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Mechanisms of aging, age-associated diseases, and lifespan determination.Experimental biology and medicine (Maywood, N.J.) · 2020
    Article
  8. 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

6 authors at 1 institution in 1 country.

Wei-Hua LeeDepartment of Medical Genetics, University of Wisconsin-Madison, Madison, WI 53706, USA.
Vijesh J BhuteDepartment of Chemical and Biological Engineering, University of Wisconsin-Madison, Madison, WI 53706, USA.
Hitoshi HiguchiDepartment of Medical Genetics, University of Wisconsin-Madison, Madison, WI 53706, USA.ORCID 0000-0002-8600-7793
Sakae IkedaDepartment of Medical Genetics, University of Wisconsin-Madison, Madison, WI 53706, USA.
Sean P PalecekDepartment of Chemical and Biological Engineering, University of Wisconsin-Madison, Madison, WI 53706, USA.
Akihiro IkedaDepartment of Medical Genetics, University of Wisconsin-Madison, Madison, WI 53706, USA.ORCID 0000-0001-8440-3891
University of Wisconsin–Madison · US

Funding

Molecular Genetics of Age-Dependent Retinal DegenerationR01EY022086 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI AKIHIRO IKEDA · 2012 to 2026
$6.1M
A Multi-Omics Approach to Discover Metabolic Critical Quality Attributes for Cardiomyocyte BiomanufacturingR01HL148059 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI PALECEK, SEAN P · 2019 to 2022
$1.5M
NEI NIH HHS R01 EY022086NHLBI NIH HHS R01 HL148059
6 · The paper itself

Abstract

impact statementMitochondria are dynamic organelles undergoing fission and fusion. Proper regulation of this process is important for healthy aging process, as aberrant mitochondrial dynamics are associated with several age-related diseases/pathologies. However, it is not well understood how imbalanced mitochondrial dynamics may lead to those diseases and pathologies. Here, we aimed to determine metabolic alterations in tissues and cells from mouse models with over-fused (fusion > fission) and over-fragmented (fusion < fission) mitochondria that display age-related disease pathologies. Our results indicated tissue-dependent sensitivity to these mitochondrial changes, and metabolic pathways likely affected by aberrant mitochondrial dynamics. This study provides new insights into how dysregulated mitochondrial dynamics could lead to functional abnormalities of tissues and cells.

Indexed as

AnimalsCells, CulturedCerebellumHippocampusMembrane ProteinsMetabolic Networks and PathwaysMetabolomeMetabolomicsMice, Inbred C57BLMitochondrial ProteinsMutationMyocardiumPrincipal Component AnalysisRetinal Pigment EpitheliumMembrane ProteinsMitochondrial ProteinsTmem135 protein, mouseheartmetabolomicsMitochondrial dynamicsmouse modelsretinal pigment epitheliumTmem135

Identifiers

PMID32515224
PMCPMC7787545
OpenAlexW3033316520

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.