Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
September 20, 2019Open Access

EPRS Regulates Proline-rich Pro-fibrotic Protein Synthesis during Cardiac Fibrosis

View Full Paper
Ask AI
Bookmark
Share

Why the study?

Critical factors and molecular mechanisms for translational control of pro-fibrotic genes during cardiac fibrosis remain unclear, prompting investigation into the role of glutamyl-prolyl-tRNA synthetase (EPRS).

Population

Human and mouse heart failure samples and mouse models

Comparison

Global or myofibroblast-specific Eprs knockout vs controls

Design

Preclinical experimental and animal model study

Authors

JWJiangbin WuKSKadiam C. Venkata SubbaiahLXLi Xie

Discussion

Loading...

Member takes

Overview

EPRS inhibition reduced fibrosis in mice; hypothesis-generating for antifibrotic therapy in human HF.

Structured PICO

P
Population
Human heart samples (17 explanted failing hearts, 8 non-failing donor hearts) and mouse models (global Eprs+/- knockout, myofibroblast-specific Eprs conditional knockout, and wild-type mice) subjected to isoproterenol (ISO) infusion or transverse aortic constriction (TAC).
I
Intervention
Genetic ablation of one Eprs allele (global or myofibroblast-specific) or pharmacological inhibition of EPRS with halofuginone (Halo).
C
Comparator
Wild-type mice, vehicle treatment, or sham operation.
O
Outcome
Cardiac fibrosis (measured by picrosirius red staining) and cardiac hypertrophy (measured by heart weight/tibia length ratio and myocyte area).surrogate

EPRS is a critical translational regulator of proline-rich pro-fibrotic genes, and its inhibition significantly reduces pathological cardiac fibrosis in heart failure models.

Cite This Study

Wu et al. (2019) studied this question.

synapsesocial.com/papers/6a849209dc9bcdcbf8c6cbdehttps://doi.org/10.1101/777490
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis2024
  2. 2Abstract Wed078: Post-transcriptional Regulation of Adrenal-Heart Crosstalk in Heart Failure with Preserved Ejection Fraction2025
  3. 3Small proline-rich protein 2B drives stress-dependent p53 degradation and fibroblast proliferation in heart failure2018 · 40 citations
  4. 4Widespread Translational Control of Fibrosis in the Human Heart by RNA-Binding Proteins2019 · 129 citations
  5. 5Small proline‐rich repeat 3 is a novel coordinator of PDGFRβ and integrin β1 crosstalk to augment proliferation and matrix synthesis by cardiac fibroblasts2020 · 33 citations