Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
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...

You might also read

Related Articles

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

Sort by
Same author

Human neural stem cells derived from fetal human brain communicate with each other and rescue ischemic neuronal cells through tunneling nanotubes.

Cell death & disease·2024
Same author

Homogeneity assessment of the SuperCam calibration targets onboard rover perseverance.

Analytica chimica acta·2022
Same author

SuperCam Calibration Targets: Design and Development.

Space science reviews·2020
Same author

How the use of surgical masks during COVID-19 pandemic can induce skin effects.

Journal of the European Academy of Dermatology and Venereology : JEADV·2020
Same author

Pre-launch radiometric calibration of the infrared spectrometer onboard SuperCam for the Mars2020 rover.

The Review of scientific instruments·2020
Same author

CROCC-mutated rhabdoid colorectal carcinoma showing in intercellular spaces lamellipodia and cellular projections revealed by electron microscopy.

Virchows Archiv : an international journal of pathology·2019

Related Experiment Video

Updated: Jul 8, 2026

Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor
06:26

Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor

Published on: April 1, 2011

Calcium and cell death: the mitochondrial connection.

P Bernardi1, A Rasola

  • 1Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, 35121 Padova, Italy.

Sub-Cellular Biochemistry
|January 16, 2008
PubMed
Summary

Cellular calcium signals trigger mitochondrial calcium uptake, impacting metabolism. However, excessive mitochondrial calcium can induce cell death by opening the permeability transition pore (PTP).

Area of Science:

  • Mitochondrial physiology
  • Cellular signaling
  • Pathophysiology

Background:

  • Physiological stimuli increase cytosolic calcium ([Ca2+]c), leading to mitochondrial calcium uptake and elevated matrix calcium ([Ca2+]m).
  • Mitochondria buffer and shape cellular calcium signals, influencing metabolic regulation via Ca2+-sensitive enzymes.
  • Despite low-affinity uptake systems, mitochondrial calcium rises to levels activating metabolic pathways.

Purpose of the Study:

  • To investigate the dual role of mitochondrial calcium in metabolic regulation and cell death.
  • To understand the transition of calcium signaling from a physiological to a pathological effector.
  • To explore the mechanisms underlying calcium overload-induced cell death.

Main Methods:

  • Observational studies on cellular calcium dynamics.

More Related Videos

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

Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay
05:53

Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay

Published on: May 1, 2018

Related Experiment Videos

Last Updated: Jul 8, 2026

Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor
06:26

Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor

Published on: April 1, 2011

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

Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay
05:53

Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay

Published on: May 1, 2018

  • In vitro analysis of mitochondrial calcium uptake kinetics.
  • Investigation of mitochondrial permeability transition pore (PTP) opening.
  • Main Results:

    • Mitochondrial calcium uptake is a rapid response to cytosolic calcium increases.
    • Elevated mitochondrial calcium ([Ca2+]m) activates Krebs cycle enzymes.
    • Mitochondrial calcium overload can trigger opening of the permeability transition pore (PTP), leading to cell death.

    Conclusions:

    • Mitochondria play a critical role in regulating cellular calcium signals and metabolism.
    • Dysregulation of mitochondrial calcium homeostasis can shift calcium's role from beneficial to detrimental.
    • Understanding the pathological role of mitochondrial calcium is crucial for developing new disease treatments.