Evidence map›Paper›PMID 39662751›Full record

ArticleInternational journal of cardiology2025

Cardiac matrix-bound Nanovesicles provide insight into mechanisms of clinical heart disease progression to failure.

Madeline Cramer, Matt Borrelli, Lisa Mathews, Marley Dewey, William Schwarzmann, Vishal Soman, John Sembrat, Mauricio Rojas, Charlie McTiernan, Uma Chandran and 3 more

Abstract read
In one paragraph

Article in International journal of cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
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

13 authors.

Madeline CramerDepartment of Surgery, Pittsburgh, PA 15213, USA; McGowan Institute for Regenerative Medicine, Pittsburgh, PA 15213, USA.
Matt BorrelliMcGowan Institute for Regenerative Medicine, Pittsburgh, PA 15213, USA; Department of Chemical Engineering, University of Pittsburgh, 940 Benedum Hall, 3700 O'Hara Street, Pittsburgh, PA 15213, USA.
Lisa MathewsDepartment of Surgery, Pittsburgh, PA 15213, USA; Thomas E. Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Marley DeweyDepartment of Surgery, Pittsburgh, PA 15213, USA; McGowan Institute for Regenerative Medicine, Pittsburgh, PA 15213, USA; Department of Bioengineering, University of California Santa Barbara, Santa Barbara, CA 93106, USA.
William SchwarzmannDepartment of Biomedical Informatics, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Vishal SomanDepartment of Biomedical Informatics, University of Pittsburgh, Pittsburgh, PA 15213, USA.
John SembratDepartment of Medicine Division of Pulmonary, Critical Care, and Sleep Medicine, The Ohio State University, USA.
Mauricio RojasDepartment of Medicine Division of Pulmonary, Critical Care, and Sleep Medicine, The Ohio State University, USA.
Charlie McTiernanDepartment of Medicine Division of Pulmonary, Critical Care, and Sleep Medicine, The Ohio State University, USA.
Uma ChandranDepartment of Biomedical Informatics, University of Pittsburgh, Pittsburgh, PA 15213, USA.
George S HusseyMcGowan Institute for Regenerative Medicine, Pittsburgh, PA 15213, USA; Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Stephen F BadylakDepartment of Surgery, Pittsburgh, PA 15213, USA; McGowan Institute for Regenerative Medicine, Pittsburgh, PA 15213, USA.
Heth R TurnquistDepartment of Surgery, Pittsburgh, PA 15213, USA; McGowan Institute for Regenerative Medicine, Pittsburgh, PA 15213, USA; Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. Electronic address: het5@pitt.edu.

Funding

NRSA Training CoreTL1TR001858 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI RADOMSKI, THOMAS, RUBIO, DORIS M · 2016 to 2025
$11.1M
Cardiovascular Bioengineering Training ProgramT32HL076124 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SANJEEV G SHROFF · 2005 to 2026
$7.0M
Immunoregulatory Mechanisms of IL-33 in Heart TransplantationR01HL122489 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Heth R Turnquist · 2015 to 2026
$4.9M
Mechanisms of functional skeletal muscle repair: critical role of matrix associated IL-33R01AR073527 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BADYLAK, STEPHEN F., TURNQUIST, HETH R · 2018 to 2022
$2.6M
Systems Metabolomics for HCC Biomarker DiscoveryR01GM123766 · NIGMS · GEORGETOWN UNIVERSITY · PI RESSOM, HABTOM W · 2017 to 2021
$1.5M
Understanding and countering mechanisms underlying IL-33-driven support of graft-vs. host diseaseR56AI139327 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TURNQUIST, HETH R · 2019 to 2019
$372k
NCATS NIH HHS TL1 TR001858NHLBI NIH HHS R01 HL122489NHLBI NIH HHS T32 HL076124NIAID NIH HHS R56 AI139327NIAMS NIH HHS R01 AR073527NIGMS NIH HHS R01 GM123766
6 · The paper itself

Abstract

aimsRemodeling of the extracellular matrix (ECM) is critical for effective wound healing and maintaining organ homeostasis. The ECM of soft tissues, including cardiac, contains embedded nanovesicles; or matrix-bound nanovesicles (MBV). The luminal cargo of MBV consists of lipids, microRNAs (miRNAs), and proteins that influence the function of immune and stromal cells. ECM remodeling is extensive during heart disease, yet it is unknown if MBV are altered during the development of heart disease. We conducted the present study to answer this question. METHODS AND

resultsMBV were isolated from de-identified human left ventricle (LV) tissue samples from: 1) non-ischemic, failing hearts (failing) and 2) non-failing, non-ischemic hearts (control). MBV morphology was analyzed and the protein and miRNA cargo were quantified. Immunomodulatory capacity of MBV was assessed on macrophages. Failing and control heart tissue had similar concentrations of MBV, however, their size and cargo differed. MBV from failing tissue had increased levels of Apolipoprotein A-1 and decreased levels of C-Reactive Protein. Over 600 unique miRNA were detected. Of these, 5 % showed significantly different levels, with most being downregulated in MBV from failing heart tissue. Ex vivo stimulation of human macrophages with MBV isolated from control ventricular tissue, but not failing ventricles, induced gene expression suggesting increased reparative functions.

conclusionThese data reveal that MBV are present within the human heart and suggests that disease progression alters MBV cargo (lipids, microRNAs, and proteins). Furthermore, it is suggested that alterations in local MBV cargo may perpetuate pathology when their capacity to modulate reparative immune cells is diminished.

Indexed as

Disease ProgressionExtracellular MatrixExtracellular VesiclesHeart FailureMyocardiumAgedFemaleHumansMaleMicroRNAsMiddle AgedMicroRNAsExtracellular matrixExtracellular vesiclesHeart failureImmunomodulationMacrophages

Identifiers

PMID39662751
PMCPMC12051099

What Socratic holds

Textmetadata
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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 Socratic graph.