Evidence map›Paper›PMID 34233296›Full record

ArticleAging2021

IGF IIRα-triggered pathological manifestations in the heart aggravate renal inflammation in STZ-induced type-I diabetes rats.

Henry Cherng-Han Lin, Catherine Reena Paul, Chia-Hua Kuo, Yung-Hsien Chang, William Shao-Tsu Chen, Tsung-Jung Ho, Cecilia Hsuan Day, Vijaya Padma Viswanadha, Yuhsin Tsai, Chih-Yang Huang

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

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 40% 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 1 citations in OpenAlex.

  1. Pooled it
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

10 authors at 8 institutions in 2 countries.

Henry Cherng-Han LinGraduate Institute of Chinese Medicine, China Medical University, Taichung 404, Taiwan.
Catherine Reena PaulCardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 97004, Taiwan.
Chia-Hua KuoLaboratory of Exercise Biochemistry, University of Taipei, Taipei 11153, Taiwan.
Yung-Hsien ChangDepartment of Chinese Medicine, China Medical University Hospital, China Medical University, Taichung 404, Taiwan.
William Shao-Tsu ChenDepartment of Psychiatry, Tzu Chi General Hospital, Hualien 97004, Taiwan.
Tsung-Jung HoDepartment of Chinese Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Tzu Chi University, Hualien 97004, Taiwan.
Cecilia Hsuan DayDepartment of Nursing, MeiHo University, Pingtung 912, Taiwan.
Vijaya Padma ViswanadhaDepartment of Biotechnology, Bharathiar University, Coimbatore 641046, India.
Yuhsin TsaiGraduate Institute of Chinese Medicine, China Medical University, Taichung 41354, Taiwan.
Chih-Yang HuangCardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 97004, Taiwan.
China Medical University · TWTzu Chi Foundation · TWAsia University · TWBharathiar University · INChina Medical University Hospital · TWMeiho University · TWTzu Chi University · TWUniversity of Taipei · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathological manifestations in either heart or kidney impact the function of the other and form the basis for the development of cardiorenal syndrome. However, the mechanism or factors involved in such scenario are not completely elucidated. In our study, to find the correlation between late fetal gene expression in diabetic hearts and their influence on diabetic nephropathy, we created a rat model with cardiac specific overexpression of IGF-IIRα, which is an alternative splicing variant of IGFIIR, expressed in pathological hearts. In this study, transgenic rats over expressing cardiac specific IGF-IIRα and non-transgenic animal models established in SD rats were administered with single dose of streptozotocin (STZ, 55 mg/Kg) to induce Type I diabetes. The correlation between IGF-IIRα and kidney damages were further determined based on their intensity of damage in the kidneys. The results show that cardiac specific overexpression of IGF-IIRα elevates the diabetes associated inflammation and morphological changes in the kidneys. The diabetic transgenic rats showed advancement in the pathological features such a renal tubular damage, collagen accumulation and enhancement in STAT3 associated mechanism of renal fibrosis. The results therefore show that that IGF-IIRα expression in the heart during pathological condition may worsen symptoms of diabetic nephropathy in rats.

Indexed as

AnimalsApoptosisCollagenDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetic CardiomyopathiesDiabetic NephropathiesFibrosisGene Expression RegulationKidneyKidney TubulesMaleMyocardiumRatsRats, Sprague-DawleyRats, TransgenicCollagenReceptor, IGF Type 2Stat3 protein, ratSTAT3 Transcription Factorcardiac stresscardiorenal syndromediabetesembryonic generenal fibrosis

Identifiers

PMID34233296
PMCPMC8312445
OpenAlexW3181485832

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.