Evidence map›Paper›PMID 38566123›Full record

ArticleCardiovascular diabetology2024

Irisin attenuates type 1 diabetic cardiomyopathy by anti-ferroptosis via SIRT1-mediated deacetylation of p53.

Yuan-Juan Tang, Zhen Zhang, Tong Yan, Ken Chen, Guo-Fan Xu, Shi-Qiang Xiong, Dai-Qian Wu, Jie Chen, Pedro A Jose, Chun-Yu Zeng and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
24.2field-weighted citation impact, top 1% 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

63 citing papers in PubMed, 74 citations in OpenAlex.

  1. SIRT1 in Neurodegenerative Diseases: Molecular Mechanisms, Disease Relevance, and Therapeutic Potential.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  7. Protective Effect ofCurrent issues in molecular biology · 2026
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3 more citing papers are in PubMed but not listed here.

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 5 institutions in 3 countries.

Yuan-Juan Tang *Department of Cardiology, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, Chengdu, 610031, China.
Zhen Zhang *Department of Cardiology, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, Chengdu, 610031, China.
Tong YanDepartment of Cardiology, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, Chengdu, 610031, China.
Ken ChenDepartment of Cardiology, Daping Hospital, Third Military Medical University (Army Medical University), Chongqing, 400042, China.
Guo-Fan XuDepartment of Cardiology and Endocrinolgy, Pangang Group Chengdu Hospital, Chengdu, 610066, China.
Shi-Qiang XiongDepartment of Cardiology, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, Chengdu, 610031, China.
Dai-Qian WuDepartment of Cardiology, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, Chengdu, 610031, China.
Jie ChenDepartment of Cardiovascular Surgery, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, Chengdu, 610031, China.
Pedro A JoseDivision of Renal Diseases & Hypertension, Department of Medicine and Department of Physiology/Pharmacology, The George Washington University School of Medicine & Health Sciences, Washington, DC, 20037, USA.
Chun-Yu ZengDepartment of Cardiology, Daping Hospital, Third Military Medical University (Army Medical University), Chongqing, 400042, China. chunyuzeng01@163.com.
Jin-Juan FuDepartment of Cardiology, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, Chengdu, 610031, China. fujinjuan@swjtu.edu.cn.
Third People's Hospital of Chengdu · CNSouthwest Jiaotong University · CNArmy Medical University · CNGeorge Washington University · USMinistry of Education · TH

Funding

Spatiotemporal transregulation of D1-like angiotensin receptors in genetically...P01HL074940 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GILDEA, JOHN JOSEPH · 2004 to 2020
$31.8M
RENAL DOPAMINE-1 RECEPTOR DEFECT IN HYPERTENSIONR01DK039308 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI JOSE, PEDRO A. · 1987 to 2020
$7.4M
Renal Dopamine Receptor & RegulationR37HL023081 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI JOSE, PEDRO A. · 2007 to 2016
$4.3M
D2 receptor variation and renal dysfunctionR01DK134574 · NIDDK · GEORGE WASHINGTON UNIVERSITY · PI Pedro A. Jose · 2023 to 2026
$2.8M
Lipid rafts, dopamine 1 receptor, and hypertensionR01DK119652 · NIDDK · GEORGE WASHINGTON UNIVERSITY · PI JOSE, PEDRO A. · 2020 to 2023
$2.6M
NHLBI NIH HHS P01 HL074940NHLBI NIH HHS R37 HL023081NIDDK NIH HHS R01 DK039308NIDDK NIH HHS R01 DK119652NIDDK NIH HHS R01 DK134574NIH HHS 5R01DK039308-31, 7R37HL023081-37, 5P01HL074940-11, 1R01DK119652-05, and 1R01DK134574-01
6 · The paper itself

Abstract

backgroundDiabetic cardiomyopathy (DCM) is a serious complication in patients with type 1 diabetes mellitus (T1DM), which still lacks adequate therapy. Irisin, a cleavage peptide off fibronectin type III domain-containing 5, has been shown to preserve cardiac function in cardiac ischemia-reperfusion injury. Whether or not irisin plays a cardioprotective role in DCM is not known. METHODS AND

resultsT1DM was induced by multiple low-dose intraperitoneal injections of streptozotocin (STZ). Our current study showed that irisin expression/level was lower in the heart and serum of mice with STZ-induced TIDM. Irisin supplementation by intraperitoneal injection improved the impaired cardiac function in mice with DCM, which was ascribed to the inhibition of ferroptosis, because the increased ferroptosis, associated with increased cardiac malondialdehyde (MDA), decreased reduced glutathione (GSH) and protein expressions of solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), was ameliorated by irisin. In the presence of erastin, a ferroptosis inducer, the irisin-mediated protective effects were blocked. Mechanistically, irisin treatment increased Sirtuin 1 (SIRT1) and decreased p53 K382 acetylation, which decreased p53 protein expression by increasing its degradation, consequently upregulated SLC7A11 and GPX4 expressions. Thus, irisin-mediated reduction in p53 decreases ferroptosis and protects cardiomyocytes against injury due to high glucose.

conclusionThis study demonstrated that irisin could improve cardiac function by suppressing ferroptosis in T1DM via the SIRT1-p53-SLC7A11/GPX4 pathway. Irisin may be a therapeutic approach in the management of T1DM-induced cardiomyopathy.

Indexed as

Diabetes Mellitus, Type 1Diabetic CardiomyopathiesFerroptosisAnimalsFibronectinsHumansMiceMyocytes, CardiacSirtuin 1Tumor Suppressor Protein p53FibronectinsSIRT1 protein, humanSirtuin 1Tumor Suppressor Protein p53FerroptosisIrisinp53SIRT1Type 1 diabetic cardiomyopathy

Identifiers

PMID38566123
PMCPMC10985893
OpenAlexW4393433515

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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.