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Related Concept Videos

Autophagy01:27

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,...
Autophagic Cell Death01:18

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 pro-apoptotic...
Delivery Pathways to the Lysosome01:36

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...
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
Cellular Injury V: Apoptosis and Autophagy01:22

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...

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Related Experiment Video

Updated: May 23, 2026

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice
08:40

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice

Published on: November 22, 2017

Mitochondrial Ca(2+) signals in autophagy.

César Cárdenas1, J Kevin Foskett

  • 1Department of Physiology, University of Pennsylvania, Philadelphia, PA 19104-6085, USA.

Cell Calcium
|March 31, 2012
PubMed
Summary

Calcium signaling regulates autophagy through both mTOR-dependent and independent pathways. Constitutive calcium transfer to mitochondria via InsP3R suppresses autophagy, while its absence activates pro-survival autophagy.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Macroautophagy (autophagy) is a conserved cellular recycling process regulated by signaling pathways.
  • The mammalian target of rapamycin (mTOR) is a key regulator in the canonical autophagy pathway.
  • Cytoplasmic calcium (Ca2+) signaling influences autophagy through both canonical and non-canonical pathways.

Purpose of the Study:

  • To review the regulation of autophagy by Ca2+ signaling.
  • To focus on an mTOR-independent pathway involving the inositol trisphosphate receptor (InsP3R) and mitochondrial Ca2+ signaling.
  • To elucidate the role of InsP3R-mediated Ca2+ transfer to mitochondria in autophagy suppression.

Main Methods:

  • Review of existing literature on autophagy regulation.

More Related Videos

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome
07:56

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Published on: November 30, 2022

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells
08:29

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells

Published on: April 27, 2018

Related Experiment Videos

Last Updated: May 23, 2026

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice
08:40

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice

Published on: November 22, 2017

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome
07:56

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Published on: November 30, 2022

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells
08:29

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells

Published on: April 27, 2018

  • Focus on the interplay between Ca2+ signaling, InsP3R, mitochondria, and mTOR-independent pathways.
  • Analysis of the consequences of impaired Ca2+ transfer to mitochondria on cellular metabolism and autophagy.

    • Main Results:

    • Constitutive InsP3R-mediated Ca2+ transfer to mitochondria suppresses autophagy in nutrient-rich conditions.
    • Absence of this Ca2+ transfer leads to metabolic compromise and activation of AMPK.
    • AMPK activation triggers mTOR-independent pro-survival autophagy.

    Conclusions:

    • Mitochondrial Ca2+ signaling via InsP3R is crucial for suppressing autophagy.
    • This Ca2+ transfer is essential for efficient mitochondrial respiration and cellular bioenergetics.
    • Dysregulation of InsP3R-mediated Ca2+ signaling impacts autophagy and cellular energy homeostasis.