Evidence map›Paper›PMID 31886288›Full record

ArticleJournal of diabetes research2019

Exendin-4 Protects against Hyperglycemia-Induced Cardiomyocyte Pyroptosis via the AMPK-TXNIP Pathway.

Hong Wei, Rui Bu, Qinghui Yang, Jing Jia, Tao Li, Qiuping Wang, Yanjun Chen

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

Article in Journal of diabetes research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 90 citations in OpenAlex.

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  18. The Role of Pyroptosis in Coronary Heart Disease.Anatolian journal of cardiology · 2024
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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

7 authors at 2 institutions in 1 country.

Hong WeiDepartment of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Rui BuDepartment of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Qinghui YangDepartment of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Jing JiaDepartment of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Tao LiDepartment of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Qiuping WangDepartment of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Yanjun ChenDepartment of Cardiology, Peking University Shenzhen Hospital, Shenzhen, China.ORCID https://orcid.org/0000-0001-9030-5673
Harbin Medical University · CNPeking University Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic cardiomyopathy is a common cardiac condition in patients with diabetes mellitus, which results in cardiac hypertrophy and subsequent heart failure. Chronic inflammation in the diabetic heart results in loss of cardiomyocytes and subsequentially cardiac dysfunction. Accumulated evidence implicated pyroptosis as a vital contributor to the hyperglycemia-induced cardiac inflammatory response. Exendin-4, a GLP analog, promotes survival of cardiomyocytes in cardiovascular diseases, including diabetic cardiomyopathy. However, the role of Exendin-4 in cardiac pyroptosis remains to be elucidated. Our study revealed that Exendin-4 treatment protected against heart remolding and dysfunction and attenuated cardiac inflammation in high-fat diet-fed rats. The activity of caspase-1 and production of pyroptotic cytokines were significantly inhibited by Exendin-4 treatment in the diabetic heart and in high glucose-treated cardiomyocytes as well. In an effort to understand the signaling mechanisms underlying the antipyroptotic property of Exendin-4, we found that blockade of AMPK, an oxidative stress sensor, activity diminished the antipyroptotic property of Exendin-4. Phosphorylation of AMPK resulted in degeneration of TXNIP that promoted the activation of the NLRP3 inflammasome. Exendin-4 treatment decreased the protein level of TXNIP. Moreover, RNA silencing of TXNIP mimicked the antipyroptotic actions of Exendin-4. These findings promoted us to propose a new signaling pathway mediating cardioprotective effect of Exendin-4 under hyperglycemic conditions: Exendin-4 → ROS↓ → pAMPK↑ → TXNIP↓ → caspase-1↓ → IL-1

Indexed as

AMP-Activated Protein KinasesAnimalsBiomarkersBlood GlucoseCarrier ProteinsCaspase 1Cells, CulturedDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic CardiomyopathiesExenatideHypoglycemic AgentsIncretinsInterleukin-18Interleukin-1betaMice, Inbred C57BLAMP-Activated Protein KinasesBiomarkersBlood GlucoseCarrier ProteinsCasp1 protein, mouseCaspase 1ExenatideHypoglycemic AgentsIL1B protein, mouseIncretinsInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReactive Oxygen SpeciesThioredoxinsTxnip protein, mouse

Identifiers

PMID31886288
PMCPMC6925927
OpenAlexW2993303703

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.