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Related Concept Videos

Role of Septins01:02

Role of Septins

2.1K
Septins are the recently discovered fourth major protein component of the cytoskeleton, along with microfilaments, microtubules, and intermediate filaments. These proteins can associate with other cytoskeletal filaments and carry out varied roles or can be free-floating in the cytoplasm.
Cellular Functions of Septins
Recent studies have revealed the multifaceted roles of septins in various cellular processes such as cytokinesis, ciliogenesis, and neurogenesis. Septins act as scaffolds and...
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Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Updated: Jan 17, 2026

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Septin4 Regulates Cardiac Fibrosis After Pressure Overload.

Doğacan Yücel1,2, Natalia Ferreira de Araujo2, Fernando Souza-Neto2

  • 1Department of Integrative Biology and Physiology (D.Y., D.W.T., J.H.v.B.), University of Minnesota, Minneapolis.

Circulation Research
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PubMed
Summary
This summary is machine-generated.

Septin4 (Sept4) deficiency protects the heart from injury by reducing fibrosis and cardiomyocyte apoptosis. This highlights Sept4 as a key target for preventing heart failure progression.

Keywords:
cardiovascular diseaseconstrictionfibrosisheart failuremyofibroblast

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Fibrosis Research

Background:

  • Cardiac remodeling post-injury can lead to heart failure.
  • Septin4 (Sept4) is involved in regeneration and apoptosis in other organs.
  • The role of Sept4 in cardiac stress response is currently unknown.

Purpose of the Study:

  • To investigate the role of Sept4 in cardiac remodeling and response to injury.
  • To determine if Sept4 deficiency confers protection against cardiac stress.

Main Methods:

  • Utilized wild-type and Sept4 knockout mice subjected to transverse aortic constriction.
  • Generated fibroblast-specific Sept4 conditional knockout mice.
  • Assessed cardiac function, apoptosis, fibrosis, and extracellular matrix deposition at various time points.

Main Results:

  • Sept4 knockout mice maintained normal cardiac function and reduced cardiomyocyte apoptosis after injury.
  • Knockout hearts showed decreased fibrosis and extracellular matrix deposition.
  • Sept4 deficiency altered calcineurin-dependent signaling in fibroblasts, reducing myofibroblast activation.

Conclusions:

  • Sept4 is a critical regulator of cardiac extracellular matrix remodeling.
  • Sept4 controls fibroblast to myofibroblast conversion via calcineurin-dependent pathways.
  • Targeting Sept4 may offer a therapeutic strategy for heart failure.