Video Experimental Relacionado

Updated: Mar 25, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

La autofagia mitocondrial dependiente de Drp1 juega un papel protector contra la disfunción mitocondrial inducida por

Akihiro Shirakabe¹, Peiyong Zhai¹, Yoshiyuki Ikeda¹

¹From Department of Cell Biology and Molecular Medicine, Rutgers-New Jersey Medical School, Newark (A.S., P.Z., Y.I., T.S., Y.M., J.S.); Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan (Y.I.); Department of Medicine and Bioregulatory Science, Kyushu University, Fukuoka, Japan (M.N.); Division of Cardiovascular Surgery, Department of Surgery, Veterans General Hospital, National Yang-Ming University School of Medicine, Taiwan (C.-P.H.); Department of Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan (K.E.); Department of Cardiovascular Research, Development, and Translational Medicine, Graduate School of Medical Science, Kyushu University Hospital, Fukuoka, Japan (K.E.); and Center for Autophagy Research, Department of Internal Medicine, and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas (B.L.).

|February 27, 2016

Resumen

La autofagia mitocondrial se activa transitoriamente y luego se desregula en la insuficiencia cardíaca. Su desregulación conduce a la disfunción cardíaca, pero la restauración de la autofagia mitocondrial puede mejorar los resultados en la sobrecarga de presión.

Área de la Ciencia:

Cardiología
Biología celular
La medicina molecular

Sus antecedentes:

La autofagia mitocondrial es crucial para el control de calidad de los cardiomiocitos.
Su papel en la hipertrofia cardíaca sigue sin estar claro.

Objetivo del estudio:

Investigar el papel y la importancia de la autofagia mitocondrial en la hipertrofia cardíaca y la insuficiencia cardíaca.
Para explorar el potencial terapéutico de modular la autofagia mitocondrial.

Principales métodos:

Los ratones se sometieron a una constricción aórtica transversal (TAC) para inducir la hipertrofia cardíaca.
La autofagia mitocondrial se evaluó mediante microscopía electrónica y marcadores específicos.
Se analizaron la expresión y función de los genes Drp1 y Beclin 1.
La inducción farmacológica de la autofagia se realizó con Tat-Beclin 1.

Principales resultados:

TAC indujo hipertrofia cardíaca, fracción de eyección reducida y insuficiencia cardíaca.
La autofagia mitocondrial se activó transitoriamente después de la TAC (3-7 días) pero posteriormente se desreguló.
La deficiencia de Drp1 abolió la autofagia mitocondrial y empeoró la disfunción cardíaca.
Tat-Beclin 1 restauró parcialmente la autofagia mitocondrial y atenuó la insuficiencia cardíaca.

Conclusiones:

La autofagia mitocondrial se activa transitoriamente y luego se desregula durante la insuficiencia cardíaca inducida por sobrecarga de presión.
La desregulación de la autofagia mitocondrial contribuye a la disfunción cardíaca.
La restauración de la autofagia mitocondrial muestra una promesa terapéutica para la insuficiencia cardíaca.

Palabras clave:

Proteína Drp1, ratón La autofagia hipertrofía Las mitocondrias

Más Videos Relacionados

Sensitive Measurement of Mitophagy by Flow Cytometry Using the pH-dependent Fluorescent Reporter mt-Keima

Sensitive Measurement of Mitophagy by Flow Cytometry Using the pH-dependent Fluorescent Reporter mt-Keima

Published on: August 12, 2018

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Published on: November 30, 2022

Videos de Conceptos Relacionados

Heart Failure II: Pathophysiology

Heart Failure II: Pathophysiology

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...

Pathophysiology of Heart Failure

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...

Autophagy

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...

Cardiomyopathy II: Dilated Cardiomyopathy

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...