Evidence map›Paper›PMID 33275651›Full record

ArticleInvestigative ophthalmology & visual science2020

Mitochondria as a Platform for Dictating the Cell Fate of Cultured Human Corneal Endothelial Cells.

Kohsaku Numa, Morio Ueno, Tomoko Fujita, Koji Ueda, Nao Hiramoto, Atushi Mukai, Yuichi Tokuda, Masakazu Nakano, Chie Sotozono, Shigeru Kinoshita and 1 more

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  3. Dysregulation of Mitochondrial Function in Cancer Cells.International journal of molecular sciences · 2025
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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

11 authors at 2 institutions in 1 country.

Kohsaku NumaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Morio UenoDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Tomoko FujitaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Koji UedaProject for Personalized Cancer Medicine, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Nao HiramotoDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Atushi MukaiDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Yuichi TokudaDepartment of Genomic Medical Sciences, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Masakazu NakanoDepartment of Genomic Medical Sciences, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Chie SotozonoDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Shigeru KinoshitaDepartment of Frontier Medical Science and Technology for Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Junji HamuroDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kyoto Prefectural University of Medicine · JPJapanese Foundation For Cancer Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Aiming to clarify the role of mitochondria in cell fate decision of cultured human corneal endothelial cell (cHCEC) subpopulations. Methods: The mitochondrial respiratory ability were examined with Mito stress and Mito fuel flex test assays using an extracellular flux analyzer (XFe24; Agilent Technologies; Santa Clara, CA) for human corneal endothelium tissues, mature cHCECs and a variety of cell state transitioned cHCECs. Tricarboxylic acid cycle and acetyl-coenzyme A-related enzymes was analyzed by proteomics for cell lysates using liquid chromatography-tandem mass spectrometry for cHCEC subpopulations. Results: The maximum oxygen consumption rate was found to become stable depending on the maturation of cHCECs. In the Mito stress tests, culture supplements, epidermal growth factor, SB203580, and SB431543 significantly repressed oxygen consumption rate, whereas a Rho-associated protein kinase inhibitor Y-27632 increased. Tricarboxylic acid cycle and mitochondria acetyl-coenzyme A-related enzymes were selectively upregulated in mature cHCECs, but not in cell state transitioned cHCECs. The maximum oxygen consumption rate was found to be higher in healthy human corneal endothelium tissues than those with deeply reduced cell density. An upregulated tricarboxylic acid cycle was linked with metabolic rewiring converting cHCECs to acquire the mitochondria-dependent oxidative phenotype. Conclusions: Mitochondrial metabolic intermediates and energy metabolism are tightly linked to the endothelial cell fate and function. These findings will help us to standardize a protocol for endothelial cell injection.

Indexed as

Acetyl Coenzyme ACells, CulturedCitric Acid CycleEndothelium, CornealGas Chromatography-Mass SpectrometryHumansMitochondriaOxygenPyruvic AcidAcetyl Coenzyme AOxygenPyruvic Acid

Identifiers

PMID33275651
PMCPMC7718813
OpenAlexW3107845659

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.