What is the clinical evidence from this study?

Population: Cardiac fibrosis. Intervention: miR-125b silencing. Primary outcome: Angiotensin II-induced perivascular and interstitial fibrosis.

What question did this study set out to answer?

This research aims to explore the role of miR-125b in cardiac fibrosis and fibroblast activation.

January 18, 2016CirculationOpen Access

MiR-125b Is Critical for Fibroblast-to-Myofibroblast Transition and Cardiac Fibrosis

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Key result

In vivo silencing of miR-125b by systemic delivery of locked nucleic acid rescued angiotensin II-induced perivascular and interstitial fibrosis.

Why the study?

Does in vivo silencing of miR-125b reduce cardiac fibrosis in murine models?

Key Points

This research aims to explore the role of miR-125b in cardiac fibrosis and fibroblast activation.
In vitro and in vivo studies to assess miR-125b's impact on cardiac fibroblasts.
Systemic delivery of locked nucleic acid for miR-125b silencing in murine cardiac fibrosis models.
RNA-sequencing to analyze gene expression profiles related to fibrosis.
MiR-125b is induced in human and murine models of cardiac fibrosis.
Silencing miR-125b rescues angiotensin II-induced fibrosis, demonstrating functional significance (P<0.05).
MiR-125b alters expression of key fibrosis-related genes, confirming its role in fibrogenesis.

Structured PICO

Does in vivo silencing of miR-125b reduce cardiac fibrosis in murine models?

Population

Fibrotic human heart samples and murine models of cardiac fibrosis (in vitro and in vivo studies)

Intervention

In vivo silencing of miR-125b by systemic delivery of locked nucleic acid

Outcome

Cardiac fibrosis (perivascular and interstitial)surrogate

miR-125b drives cardiac fibrosis by targeting apelin and inhibiting p53, and its systemic silencing rescues angiotensin II-induced fibrosis in vivo.

Discussion

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Implication

miR-125b inhibition may limit fibrosis; leaves open therapeutic translation in human cardiac disease.

Cite This Study

Nagpal et al. (2016) studied Cardiac fibrosis. miR-125b silencing was evaluated on Angiotensin II-induced perivascular and interstitial fibrosis. In vivo silencing of miR-125b by systemic delivery of locked nucleic acid rescued angiotensin II-induced perivascular and interstitial fibrosis.

synapsesocial.com/papers/6a62dbe5aca57fe965286a7d https://doi.org/10.1161/circulationaha.115.018174

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MiR-125b Is Critical for Fibroblast-to-Myofibroblast Transition and Cardiac Fibrosis

Key Points

Structured PICO

Discussion

Implication

Cite This Study

MiR-125b Is Critical for Fibroblast-to-Myofibroblast Transition and Cardiac Fibrosis

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider