Evidence map›Paper›PMID 41889994›Full record

ArticlebioRxiv : the preprint server for biology2026

T cell-derived IFNγ instructs ECM crosslinking by cardiac fibroblasts through LOXL3 in experimental cardiometabolic HFpEF.

Ramona Emig, Zachary Robbe, Celina Kley, Sasha Smolgovsky, Joshua G Travers, Robert M Blanton, Timothy A McKinsey, Lauren D Black, Pilar Alcaide

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Ramona EmigDepartment of Microbiology and Immunology, Miller School of Medicine, University of Miami, Miami, FL, USA.
Zachary RobbeDepartment of Immunology, School of Medicine, Tufts University, Boston, MA, USA.
Celina KleyGerman Centre of Cardiovascular Research, University of Heidelberg, Heidelberg, Germany.
Sasha SmolgovskyDepartment of Immunology, School of Medicine, Tufts University, Boston, MA, USA.
Joshua G TraversDepartment of Medicine, Division of Cardiology, and Consortium for Fibrosis Research & Translation, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Robert M BlantonMolecular Cardiology Research Institute, School of Medicine, Tufts University, Boston, USA.
Timothy A McKinseyDepartment of Medicine, Division of Cardiology, and Consortium for Fibrosis Research & Translation, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Lauren D BlackDepartment for Bioengineering, Tufts University, Boston, MA, USA.
Pilar AlcaideDepartment of Microbiology and Immunology, Miller School of Medicine, University of Miami, Miami, FL, USA.

Funding

Regulation of Chromatin Signaling in Heart Failure by the BRD4 Bromodomain Protein.R01HL127240 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY, SRIVASTAVA, DEEPAK · 2015 to 2022
$6.4M
Mechanisms of T cell activation in cardiac fibrosis and non-ischemic heart failureR01HL144477 · NHLBI · TUFTS UNIVERSITY BOSTON · PI ALCAIDE ALONSO, MARIA PILAR · 2019 to 2023
$3.2M
Regulation of T cell immune response in Heart Failure with Preserved Ejection FractionR01HL165725 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Maria Pilar Alcaide Alonso · 2023 to 2026
$2.5M
15-PGDH-Mediated Eicosanoid Degradation in Cardiac Fibrosis and Heart FailureR01HL171711 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI Timothy McKinsey · 2024 to 2026
$1.6M
Elucidating the Molecular Mechanisms and Cellular Specificity of HDAC Inhibitor Efficacy in Diastolic DysfunctionK99HL166708 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI TRAVERS, JOSHUA · 2023 to 2024
$214k
Exploring the Therapeutic Potential of BRD4 Extra-terminal Domain Inhibition in Cardiac Dysfunction and Remodeling. Fellow: Joshua TraversF32HL147463 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI TRAVERS, JOSHUA · 2019 to 2020
$127k
Characterizing mechanisms of T cell-mediated cardiac pathology in Heart Failure with Preserved Ejection FractionF31HL159907 · NHLBI · TUFTS UNIVERSITY BOSTON · PI SMOLGOVSKY, SANDRA · 2022 to 2023
$67k
NHLBI NIH HHS F31 HL159907NHLBI NIH HHS F32 HL147463NHLBI NIH HHS K99 HL166708NHLBI NIH HHS R01 HL127240NHLBI NIH HHS R01 HL144477NHLBI NIH HHS R01 HL165725NHLBI NIH HHS R01 HL171711
6 · The paper itself

Abstract

Background: Heart failure with preserved ejection fraction (HFpEF) is a major clinical challenge characterized by diastolic dysfunction. Left ventricular stiffening and inflammation are hallmarks of HFpEF, yet the contribution of extracellular matrix (ECM) stiffness and the immune-stromal mechanisms driving ECM stiffening in cardiometabolic HFpEF remain poorly understood. Methods: We used the murine "2-hit model" of cardiometabolic HFpEF, in which the combination of high fat diet and hypertension induced by L-NAME causes diastolic dysfunction. We evaluated diastolic function by echocardiography and ECM mechanics by uniaxial tensile testing of decellularized cardiac tissue. Functional Results: Left ventricular ECM stiffness strongly correlated with impaired diastolic function in experimental cardiometabolic HFpEF. Cardiac CD4 Conclusions: CD4

Indexed as

cardiac mechanicscardioimmunologyExtracellular matrix crosslinkingImmune-stromal

Identifiers

PMID41889994
PMCPMC13015342

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.