Evidence map›Paper›PMID 41656217›Full record

ArticleCardiovascular diabetology2026

Distinct immunometabolic signatures of type 1 versus type 2 diabetes in a murine model of myocardial infarction.

Katherine R O'Quinn, Catharyne B Wright, Mursalin Khan, Rob W Spitz, Nadiyeh Rouhi, Jemylle G Morato, Patricio A Vidal, Ana C M Omoto, Alex A da Silva, Jussara M do Carmo and 4 more

Abstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diabetology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

14 authors.

Katherine R O'QuinnDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Catharyne B WrightDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Mursalin KhanDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Rob W SpitzDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Nadiyeh RouhiDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Jemylle G MoratoDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Patricio A VidalDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Ana C M OmotoDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Alex A da SilvaDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Jussara M do CarmoDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Zhen WangDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Xuan LiDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
John E HallDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA.
Alan J MoutonDepartment of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, 39216-4505, USA. amouton@umc.edu.

Funding

The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI HALL, JOHN E · 2013 to 2022
$23.4M
Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
Pilot Projects ProgramP30GM149404 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI John E Hall · 2023 to 2026
$6.3M
American Heart Association CDA856365NHLBI Division of Intramural Research HL166737NHLBI NIH HHS T32 HL105324NIGMS NIH HHS P20 GM104357NIGMS NIH HHS P30 GM149404
6 · The paper itself

Abstract

backgroundDiabetes mellitus (DM), which consists of type I and type 2 diabetes (T1D and T2D), is a known risk factor for myocardial infarction (MI) and negatively impacts post-MI outcomes. However, the mechanisms by which DM exacerbates cardiac remodeling in T1D versus T2D have not been well defined. Here, we assessed acute and chronic post-MI outcomes in T1D and T2D mice, focusing on immune and metabolic pathways.

methodsT1D was induced in adult male mice by a single high dose of streptozotocin (STZ), and T2D induced by high fat/fructose feeding and multiple low STZ doses. Two weeks following STZ administration, MI was induced by permanent coronary artery ligation, and mice were studied at days (D) 0, 3, 7, and 28 post-MI. Cardiac function was assessed by echocardiography.

resultsCompared to non-diabetic mice, T1D and T2D mice had worse cardiac dysfunction after MI, including increased wall thinning and decreased ejection fraction, despite similar infarct sizes. T1D mice also displayed acute pulmonary congestion. By RNA-sequencing analysis, T1D and T2D mice displayed upregulation of genes associated with canonical chemokine/monocyte-mediated inflammatory pathways, and downregulation of genes associated with extracellular matrix remodeling. T1D and T2D delayed activation of M2-like (CD206+) macrophages in the heart, and impaired normal collagen and elastin deposition after MI. T2D also increased expression of genes associated with T cell activation, and increased CD8 + T cells in the infarct. T1D and T2D hearts showed signs of impaired glucose and ketone oxidation, and T1D hearts had increased markers of fatty acid oxidation. Extracted D3 cardiac macrophages from T1D and T2D mice exhibited higher basal oxygen consumption, and increased M1 markers and chemokine expression. Plasma from T1D and T2D mice increased chemokine expression (Ccl2, Ccl7, Cxcl1) in cultured bone marrow macrophages, and T2D plasma impaired mitochondrial function.

conclusionsDM promotes adverse cardiac remodeling, which is associated with activation of overlapping and unique inflammatory pathways, impaired ECM remodeling, remote metabolic remodeling, and alterations in macrophage metabolism. Our results provide novel insights into potential therapeutic pathways for DM patients suffering from MI.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Energy MetabolismMyocardial InfarctionMyocardiumVentricular RemodelingAnimalsDisease Models, AnimalInflammation MediatorsMacrophagesMaleMice, Inbred C57BLSignal TransductionTime FactorsVentricular Function, LeftInflammation MediatorsCardiac remodelingDiabetesHeart failureImmunometabolismInflammationMetabolismMyocardial infarctionObesity

Identifiers

PMID41656217
PMCPMC12983673

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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.