Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

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,...

Delivery Pathways to the Lysosome

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...

mTOR Signaling and Cancer Progression

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

Cellular Injury V: Apoptosis and Autophagy

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

Autophagic Cell Death

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Upadacitinib regulates pain-related pathways and BDNF expression in human monocyte-derived microglial-like cells.

Brain, behavior, and immunity·2025

Same author

Assessing the detection of floating plastic litter with advanced remote sensing technologies in a hydrodynamic test facility.

Scientific reports·2024

Same author

Blood and sperm traces on human hair. A study on preservation and detection after 3-month outdoor exposure.

Science & justice : journal of the Forensic Science Society·2021

Same author

A Ge.F.I. - ISFG European collaborative study on DNA identification of Cannabis sativa samples using a 13-locus multiplex STR method.

Forensic science international·2021

Same author

Psychological distress, low-income, and socio-economic vulnerability in the COVID-19 pandemic.

Public health·2021

Same author

Children with Kawasaki disease or Kawasaki-like syndrome (MIS-C/PIMS) at the time of COVID-19: are they all the same? Case series and literature review.

Reumatismo·2021

Same journal

Mitochondrial-endoplasmic reticulum interactions in lung diseases.

Cell death & disease·2026

Same journal

A ZDHHC3-USP5-PTRF axis links palmitoylation to ferroptosis-associated phenotypes in melanoma.

Cell death & disease·2026

Same journal

Small molecule-mediated activation of Notch signal transduction.

Cell death & disease·2026

Same journal

OT-55 reshapes tolerogenic BH3-mimetic-induced apoptosis toward immunogenic cell death in acute myeloid leukemia, potentiating PD-1/Tim-3 blockade.

Cell death & disease·2026

Same journal

FOXQ1 activates GLT8D2 to enhance CCL2 N-glycosylation and promote prostate cancer bone metastasis.

Cell death & disease·2026

Same journal

PCGF1-mediated bivalent promoter remodeling enables NK cell immune evasion in non-small cell lung cancer.

Cell death & disease·2026

See all related articles

Search research articles

Related Experiment Video

Updated: May 3, 2026

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry

Published on: July 21, 2017

MiR-216a: a link between endothelial dysfunction and autophagy.

R Menghini¹, V Casagrande¹, A Marino¹

¹Department of Systems Medicine, University of Rome 'Tor Vergata', Rome, Italy.

Cell Death & Disease

|February 1, 2014

Summary

This summary is machine-generated.

MicroRNA-216a impairs autophagy in aging endothelial cells, contributing to cardiovascular disease. Inhibiting miR-216a restores protective autophagy, offering a potential therapeutic target for atherosclerosis.

More Related Videos

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells

Published on: June 12, 2017

Activating Autophagy by Aerobic Exercise in Mice

Activating Autophagy by Aerobic Exercise in Mice

Published on: February 3, 2017

Related Experiment Videos

Last Updated: May 3, 2026

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry

Published on: July 21, 2017

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells

Published on: June 12, 2017

Activating Autophagy by Aerobic Exercise in Mice

Activating Autophagy by Aerobic Exercise in Mice

Published on: February 3, 2017

Area of Science:

Molecular Biology
Cell Biology
Cardiovascular Research

Background:

Endothelial dysfunction and impaired autophagy are key in aging-related cardiovascular diseases.
MicroRNA-216a (miR-216a) is upregulated during endothelial aging and computationally linked to autophagy genes BECN1 and ATG5.

Purpose of the Study:

To investigate the role of miR-216a in endothelial aging and its impact on autophagic function.
To determine if miR-216a directly targets BECN1 and ATG5 and influences autophagy in response to oxidized low-density lipoprotein (ox-LDL).

Main Methods:

Computational analysis to identify miR-216a targets.
Luciferase assays to confirm direct targeting of BECN1.
Transfection of human umbilical vein endothelial cells (HUVECs) to modulate miR-216a expression.
Stimulation with ox-LDL to induce autophagy.
Analysis of autophagy markers (LC3B) and cellular assays (cytofluorimetry, ox-LDL accumulation, monocyte adhesion).

Main Results:

miR-216a directly targets BECN1 and inversely correlates with autophagy gene expression in aging HUVECs and in vivo models.
Overexpression of miR-216a in young HUVECs repressed BECN1 and ATG5, inhibited ox-LDL-induced autophagy, and increased ox-LDL accumulation and monocyte adhesion.
Inhibition of miR-216a in aged HUVECs restored the autophagic response to ox-LDL.

Conclusions:

miR-216a regulates ox-LDL-induced autophagy in endothelial cells by controlling BECN1 levels.
miR-216a plays a significant role in the pathogenesis of cardiovascular disorders and atherosclerosis through its regulation of endothelial autophagy.