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March 26, 2018Proceedings of the National Academy of SciencesOpen Access

Small proline-rich protein 2B drives stress-dependent p53 degradation and fibroblast proliferation in heart failure

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Key result

Excessive SPRR2B expression drives pathological cardiac fibroblast accumulation in heart failure via stress-dependent p53 degradation.

Why the study?

Does SPRR2B drive stress-dependent p53 degradation and fibroblast proliferation in heart failure?

Population

Cardiac fibroblasts from human heart failure patients and a mouse model of heart disease

Design

Preclinical

Authors

RBRyan M. BurkeJLJanet K. LighthousePQPearl Quijada

Discussion

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Member takes

Overview

SPRR2B may represent a therapeutic target to limit fibrosis in heart failure; extends preclinical mechanisms but leaves clinical translation open.

Structured PICO

Does SPRR2B drive stress-dependent p53 degradation and fibroblast proliferation in heart failure?

P
Population
Cardiac fibroblasts from human heart failure patients and a mouse model of heart disease
I
Intervention
Assessment of Small proline-rich protein 2B (SPRR2B) expression and function
O
Outcome
p53 degradation and fibroblast proliferationsurrogate

SPRR2B drives pathological cardiac fibrosis in heart failure by promoting p53 degradation and fibroblast proliferation, identifying a potential novel therapeutic target.

Cite This Study

Burke et al. (2018) studied Heart failure. SPRR2B was evaluated on p53 degradation and fibroblast proliferation. Excessive SPRR2B expression in cardiac fibroblasts drives stress-dependent p53 degradation and pathological fibroblast accumulation in heart failure.

synapsesocial.com/papers/6a0a58dcfdd00ab7863dcd8ahttps://doi.org/10.1073/pnas.1717423115
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Also Consider

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  1. 1Small 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
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  3. 3Co-ordinated regulation of cell survival and cell cycle pathways by DDR2-dependent SRF transcription factor in cardiac fibroblasts2019
  4. 4Cellular Retinoic Acid–Binding Protein 2 Promotes Ischemia‐Induced Cardiac Fibroblast Activation and Fibrosis Through Suppression of MRE11‐RAD50‐NBS1–Mediated DNA Repair2026
  5. 5Signal Recognition Granule Receptor Beta Subunit Promotes Arrhythmogenic Remodeling in the Heart Failure Mice2026