Evidence map›Paper›PMID 30090653›Full record

ArticleAging and disease2018

Pkcδ Activation is Involved in ROS-Mediated Mitochondrial Dysfunction and Apoptosis in Cardiomyocytes Exposed to Advanced Glycation End Products (Ages).

Yao-Chih Yang, Cheng-Yen Tsai, Chien-Lin Chen, Chia-Hua Kuo, Chien-Wen Hou, Shi-Yann Cheng, Ritu Aneja, Chih-Yang Huang, Wei-Wen Kuo

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

Article in Aging and disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 55 citations in OpenAlex.

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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

9 authors at 5 institutions in 2 countries.

Yao-Chih Yang1Department of Biological Science and Technology, College of Biopharmaceutical and Food Sciences, China Medical University, Taiwan.
Cheng-Yen Tsai2Department of Pediatrics, China Medical University Beigang Hospital, Taiwan.
Chien-Lin Chen4Department of Life Sciences, National Chung Hsing University, Taiwan.
Chia-Hua Kuo5Laboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan.
Chien-Wen Hou5Laboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan.
Shi-Yann Cheng7Department of Medical Education and Research and Department of Obstetrics and Gynecology, China Medical University Beigang Hospital, Taiwan.
Ritu Aneja10Department of Biology, Georgia State University, Atlanta, GA 30303, USA.
Chih-Yang Huang *11Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Graduate Institute of Chinese Medical Science, School of Chinese Medicine, China Medical University, Taichung, Taiwan; Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan.
Wei-Wen Kuo *1Department of Biological Science and Technology, College of Biopharmaceutical and Food Sciences, China Medical University, Taiwan.
China Medical University · TWUniversity of Taipei · TWAsia University · TWGeorgia State University · USNational Chung Hsing University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic patients exhibit serum AGE accumulation, which is associated with reactive oxygen species (ROS) production and diabetic cardiomyopathy. ROS-induced PKCδ activation is linked to mitochondrial dysfunction in human cells. However, the role of PKCδ in cardiac and mitochondrial dysfunction caused by AGE in diabetes is still unclear. AGE-BSA-treated cardiac cells showed dose- and time-dependent cell apoptosis, ROS generation, and selective PKCδ activation, which were reversed by NAC and rotenone. Similar tendency was also observed in diabetic and obese animal hearts. Furthermore, enhanced apoptosis and reduced survival signaling by AGE-BSA or PKCδ-WT transfection were reversed by kinase-deficient (KD) of PKCδ transfection or PKCδ inhibitor, respectively, indicating that AGE-BSA-induced cardiomyocyte death is PKCδ-dependent. Increased levels of mitochondrial mass as well as mitochondrial fission by AGE-BSA or PKCδ activator were reduced by rottlerin, siPKCδ or KD transfection, indicating that the AGE-BSA-induced mitochondrial damage is PKCδ-dependent. Using super-resolution microscopy, we confirmed that PKCδ colocalized with mitochondria. Interestingly, the mitochondrial functional analysis by Seahorse XF-24 flux analyzer showed similar results. Our findings indicated that cardiac PKCδ activation mediates AGE-BSA-induced cardiomyocyte apoptosis via ROS production and may play a key role in the development of cardiac mitochondrial dysfunction in rats with diabetes and obesity.

Indexed as

advanced glycation end products (AGEs)apoptosisdiabetes mellitus (DM)mitochondrialprotein kinase C (PKC)δreactive oxygen species (ROS)

Identifiers

PMID30090653
PMCPMC6065295
OpenAlexW2885414348

What OpenQuestion holds

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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.