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May 1, 2021Diabetes Metabolic Syndrome and ObesityOpen Access

YAP knockdown reduces fibrosis and improves cardiac function in diabetic rats by decreasing CTGF and fibronectin.

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Why the study?

YAP is related to cardiovascular disease pathology, but its role in cardiac injury of diabetic cardiomyopathy is still unclear.

Does YAP knockdown reduce myocardial fibrosis and improve cardiac function in a rat model of diabetic cardiomyopathy?

Population

Diabetic cardiomyopathy rat model and primary rat cardiac fibroblasts

Comparison

Control vs DCM vs LV-SC-shRNA vs LV-YAP-shRNA

Design

Preclinical animal and in vitro laboratory study

Key result

YAP knockdown reduced myocardial fibrosis and improved cardiac function in a rat model of diabetic cardiomyopathy by decreasing the expression of CTGF and fibronectin.

Authors

MHMaomao HuHWHan WangSLShengnan Li

Discussion

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Member takes

Overview

Does not change clinical practice in diabetic cardiomyopathy; leaves open YAP as a therapeutic target pending human studies.

Structured PICO

Does YAP knockdown reduce myocardial fibrosis and improve cardiac function in a rat model of diabetic cardiomyopathy?

P
Population
Diabetic cardiomyopathy rat model and primary rat cardiac fibroblasts stimulated with high glucose
I
Intervention
YAP knockdown via lentivirus expressing YAP-shRNA (LV-YAP-shRNA)
C
Comparator
Control group, untreated DCM group, and scramble shRNA (LV-SC-shRNA) group
O
Outcome
Myocardial fibrosis, cardiac function, and expression of CTGF and fibronectinsurrogate

YAP knockdown reduces myocardial fibrosis and improves cardiac function in a rat model of diabetic cardiomyopathy, identifying YAP as a potential therapeutic target.

Cite This Study

Hu et al. (2021) studied Diabetic cardiomyopathy. YAP-shRNA vs. SC-shRNA and untreated DCM control was evaluated on Myocardial fibrosis, cardiac function, and expression of CTGF and fibronectin. YAP knockdown reduced myocardial fibrosis and improved cardiac function in a rat model of diabetic cardiomyopathy by decreasing the expression of CTGF and fibronectin.

synapsesocial.com/papers/6a0e98d920dec68b0dc841bdhttps://doi.org/10.2147/dmso.s302466
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Also Consider

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

  1. 1(Pro)renin receptor involves in myocardial fibrosis and oxidative stress in diabetic cardiomyopathy via the PRR–YAP pathway2021 · 20 citations
  2. 2Effects of (Pro)renin Receptor on Diabetic Cardiomyopathy Pathological Processes in Rats via the PRR-AMPK-YAP Pathway2021 · 25 citations
  3. 3AAV-mediated YAP expression in cardiac fibroblasts promotes inflammation and increases fibrosis2021 · 60 citations
  4. 4Knockout of C1q/tumor necrosis factor-related protein-9 aggravates cardiac fibrosis in diabetic mice by regulating YAP-mediated autophagy2024 · 5 citations
  5. 5Unraveling Diabetic Cardiomyopathy (DCM): The Critical Role of the Yap–miR-22-3p–Sirt1 Axis in the Pathogenesis of DCM2026