Evidence map›Paper›PMID 38943657›Full record

ArticleJournal of diabetes investigation2024

Regulatory T cells protect against diabetic cardiomyopathy in db/db mice.

Kai Zhang, Yunyi Li, Xiao Ge, Linlin Meng, Jing Kong, Xiao Meng

Abstract read
In one paragraph

Article in Journal of diabetes investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. The immunology of diabetic cardiomyopathy.Frontiers in endocrinology · 2025
    Review
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

6 authors.

Kai ZhangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Ministry of Education of China, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Yunyi LiThe Key Laboratory of Cardiovascular Remodeling and Function Research, Ministry of Education of China, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xiao GeThe Key Laboratory of Cardiovascular Remodeling and Function Research, Ministry of Education of China, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Linlin MengThe Key Laboratory of Cardiovascular Remodeling and Function Research, Ministry of Education of China, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Jing KongThe Key Laboratory of Cardiovascular Remodeling and Function Research, Ministry of Education of China, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xiao MengThe Key Laboratory of Cardiovascular Remodeling and Function Research, Ministry of Education of China, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.ORCID https://orcid.org/0000-0001-8086-9096

Funding

National Natural Science Foundation of China 81900321National Natural Science Foundation of China 81970319National Natural Science Foundation of China 82170361Natural Science Foundation of Shandong Province ZR2021MH100Taishan Scholars Program of Shandong Province tsqn202103170
6 · The paper itself

Abstract

AIMS/

introductionRegulatory T cells (Tregs) have protected against many cardiovascular diseases. This study was intended to explore the effect of Tregs on diabetic cardiomyopathy (DCM) using a db/db mouse model. MATERIALS AND

methodsEight-week-old male db/db mice were randomly divided into four groups: the control group, administered 200 μL phosphate-buffered saline; the small-dose Treg group, administered 10

resultsEchocardiography showed that the impaired diastolic and systolic functions were significantly improved in mice administered large-dose Tregs. Large-dose Tregs significantly ameliorated myocardial hypertrophy and fibrosis, and decreased hypertrophic gene expression and collagen deposition. The protective effects of Tregs on diabetic hearts were associated with decreased oxidative stress, inflammatory response and apoptosis. In addition, Tregs promoted the activation of the phosphatidylinositol 3-kinase-protein kinase B signaling pathway, whereas they inhibited extracellular signal-regulated kinase 1/2 and Jun N-terminal kinase phosphorylation, which might be responsible for the cardioprotective role of Tregs against DCM.

conclusionsTregs ameliorated myocardial hypertrophy and fibrosis, improved cardiac dysfunction, and protected against DCM progression in db/db mice. The mechanisms involved a decrease of inflammatory response, oxidative stress and apoptosis, which might be mediated by phosphatidylinositol 3-kinase-protein kinase B and mitogen-activated protein kinase pathways. Hence, Tregs might serve as a promising therapeutic approach for DCM treatment.

Indexed as

Diabetic CardiomyopathiesT-Lymphocytes, RegulatoryAnimalsApoptosisDiabetes Mellitus, ExperimentalDisease Models, AnimalMaleMiceOxidative StressSignal TransductionDiabetic cardiomyopathyInflammationRegulatory T cells

Identifiers

PMID38943657
PMCPMC11363098

What OpenQuestion holds

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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.