Evidence map›Paper›PMID 41258504›Full record

ArticleScientific reports2025

Macrophages lacking TSC2 have mTORC1-dependent increased GPNMB and ameliorate ventricular dysfunction/remodeling after ischemia-reperfusion.

Mohammad Keykhaei, Navid Koleini, Mariam Meddeb, David J Polhemus, Masih Tajdini, Malihe Rezaee, Qiao Huang, Tegbir Panesar, Mark J Ranek, Luigi Adamo and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Mohammad KeykhaeiDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Navid KoleiniDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Mariam MeddebDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
David J PolhemusDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Masih TajdiniDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Malihe RezaeeDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Qiao HuangDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Tegbir PanesarDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Mark J RanekDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Luigi AdamoDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
David A KassDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building Rm 858, 720 Rutland Avenue, Baltimore, MD, 21205, USA. dkass@jhmi.edu.

Funding

PATHOPHYSIOLOGY OF MYOCARDIAL DISEASEST32HL007227 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Chulan Kwon, WENDY S POST · 1985 to 2026
$21.2M
Intersection of Obesity and Heart Failure with Preserved Ejection FractionR35HL166565 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI David Alan Kass · 2023 to 2026
$4.1M
Phosphorylation of TSC2 (S1365) as a novel Regulator of mTORC1 Signaling in T CellsR01AI156274 · NIAID · JOHNS HOPKINS UNIVERSITY · PI PEARCE, ERIKA L · 2021 to 2025
$2.6M
Chip phosphorylation stimulates the degradation of mutant transthyretin to attenuate cardiac amyloidosisR01HL169273 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Mark John Ranek · 2024 to 2026
$2.1M
Myocardial-associated B lymphocytes and inflammatory injuryR01HL160716 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ADAMO, LUIGI · 2022 to 2025
$1.9M
Chip phosphorylation stimulates the degradation of mutant transthyretin to attenuate cardiac amyloidosisR56HL169273 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI RANEK, MARK JOHN · 2023 to 2023
$670k
National Institute of Allergy and Infectious Diseases AI-156274NHLBI NIH HHS HL-007227NHLBI NIH HHS HL-160716NHLBI NIH HHS HL169273NHLBI NIH HHS R01 HL160716NHLBI NIH HHS R01 HL169273NHLBI NIH HHS R35 HL166565NHLBI NIH HHS R35-HL166565NHLBI NIH HHS R56 HL169273NHLBI NIH HHS T32 HL007227NIAID NIH HHS R01 AI156274
6 · The paper itself

Abstract

Macrophages (MΦ) modulate myocardial inflammation and repair after ischemia-reperfusion (I/R) injury. The mechanistic target of rapamycin (mTOR) regulates MΦ phenotype and functionality, but studies conflict regarding its pro- or anti-inflammatory role. To test this, myeloid TSC2 depleted (MΦ

Indexed as

MacrophagesMechanistic Target of Rapamycin Complex 1Membrane GlycoproteinsMyocardial Reperfusion InjuryTuberous Sclerosis Complex 2 ProteinVentricular RemodelingAnimalsMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumSirolimusMechanistic Target of Rapamycin Complex 1Membrane GlycoproteinsSirolimusTsc2 protein, mouseTuberous Sclerosis Complex 2 ProteinHeartInnate immunityIschemiaMammalian target of rapamycinMonocyteTuberous sclerosis

Identifiers

PMID41258504
PMCPMC12630934

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.