Evidence map›Paper›PMID 24786827›Full record

ArticleCell death and differentiation2014

ANG II promotes IGF-IIR expression and cardiomyocyte apoptosis by inhibiting HSF1 via JNK activation and SIRT1 degradation.

C-Y Huang, W-W Kuo, Y-L Yeh, T-J Ho, J-Y Lin, D-Y Lin, C-H Chu, F-J Tsai, C-H Tsai, C-Y Huang

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

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 105 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

10 authors at 4 institutions in 1 country.

C-Y HuangGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan, ROC.
W-W KuoDepartment of Biological Science and Technology, China Medical University, Taichung, Taiwan, ROC.
Y-L Yeh1] Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan, ROC [2] Department of Medical Technology, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan, ROC.
T-J Ho1] Chinese Medicine Department, China Medical University Beigang Hospital, Beigang, Taiwan, ROC [2] School of Chinese Medicine, China Medical University, Taichung, Taiwan, ROC.
J-Y Lin1] Department of Medical Imaging and Radiological Science, Central Taiwan University of Science and Technology, Taichung, Taiwan, ROC [2] Department of Nursing, Central Taiwan University of Science and Technology, Taichung, Taiwan, ROC.
D-Y LinGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan, ROC.
C-H ChuGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan, ROC.
F-J TsaiSchool of Chinese Medicine, China Medical University, Taichung, Taiwan, ROC.
C-H TsaiDepartment of Healthcare Administration, Asia University, Taichung, Taiwan, ROC.
C-Y Huang1] Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan, ROC [2] School of Chinese Medicine, China Medical University, Taichung, Taiwan, ROC [3] Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan, ROC.
China Medical University · TWAsia University · TWCentral Taiwan University of Science and Technology · TWChanghua Christian Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertension-induced cardiac hypertrophy and apoptosis are major characteristics of early-stage heart failure. Our previous studies found that the activation of insulin-like growth factor receptor II (IGF-IIR) signaling was critical for hypertensive angiotensin II (ANG II)-induced cardiomyocyte apoptosis. However, the detailed mechanism by which ANG II regulates IGF-IIR in heart cells remains elusive. In this study, we found that ANG II activated its downstream kinase JNK to increase IGF-IIR expression through the ANG II receptor angiotensin type 1 receptor. JNK activation subsequently led to sirtuin 1 (SIRT1) degradation via the proteasome, thus preventing SIRT1 from deacetylating heat-shock transcription factor 1 (HSF1). The resulting increase in the acetylation of HSF1 impaired its ability to bind to the IGF-IIR promoter region (nt -748 to -585). HSF1 protected cardiomyocytes by acting as a repressor of IGF-IIR gene expression, and ANG II diminished this HSF1-mediated repression through enhanced acetylation, thus activating the IGF-IIR apoptosis pathway. Taken together, these results suggest that HSF1 represses IGF-IIR gene expression to protect cardiomyocytes. ANG II activates JNK to degrade SIRT1, resulting in HSF1 acetylation, which induces IGF-IIR expression and eventually results in cardiac hypertrophy and apoptosis. HSF1 could be a valuable target for developing treatments for cardiac diseases in hypertensive patients.

Indexed as

Angiotensin IIAnimalsApoptosisDNA-Binding ProteinsFemaleHeat Shock Transcription FactorsHumansJNK Mitogen-Activated Protein KinasesMaleMyocytes, CardiacRatsReceptor, IGF Type 2Signal TransductionSirtuin 1Transcription FactorsAngiotensin IIDNA-Binding ProteinsHeat Shock Transcription FactorsHSF1 protein, humanHsf1 protein, ratJNK Mitogen-Activated Protein KinasesReceptor, IGF Type 2Sirtuin 1Transcription Factors

Identifiers

PMID24786827
PMCPMC4085534
OpenAlexW1980304809

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.