Abstract
In the complex interplay that allows different signals to be decoded into activation of cell death, calcium (Ca2+) plays a significant role. In all eukaryotic cells, the cytosolic concentration of Ca2+ ions ([Ca2+]c) is tightly controlled by interactions among transporters, pumps, channels and binding proteins. Finely tuned changes in [Ca2+]c modulate a variety of intracellular functions ranging from muscular contraction to secretion, and disruption of Ca2+ handling leads to cell death. In this context, Ca2+ signals have been shown to affect important checkpoints of the cell death process, such as mitochondria, thus tuning the sensitivity of cells to various challenges. In this contribution, we will review (i) the evidence supporting the involvement of Ca2+ in the three major process of cell death: apoptosis, necrosis and autophagy (ii) the complex signaling interplay that allows cell death signals to be decoded into mitochondria as messages controlling cell fate.
Keywords: mitochondria, autophagy, necrosis, apoptosis, Calcium
Current Molecular Medicine
Title: Ca2+ Signaling, Mitochondria and Cell Death
Volume: 8 Issue: 2
Author(s): Paolo Pinton, Anna Romagnoli, Rosario Rizzuto and Carlotta Giorgi
Affiliation:
Keywords: mitochondria, autophagy, necrosis, apoptosis, Calcium
Abstract: In the complex interplay that allows different signals to be decoded into activation of cell death, calcium (Ca2+) plays a significant role. In all eukaryotic cells, the cytosolic concentration of Ca2+ ions ([Ca2+]c) is tightly controlled by interactions among transporters, pumps, channels and binding proteins. Finely tuned changes in [Ca2+]c modulate a variety of intracellular functions ranging from muscular contraction to secretion, and disruption of Ca2+ handling leads to cell death. In this context, Ca2+ signals have been shown to affect important checkpoints of the cell death process, such as mitochondria, thus tuning the sensitivity of cells to various challenges. In this contribution, we will review (i) the evidence supporting the involvement of Ca2+ in the three major process of cell death: apoptosis, necrosis and autophagy (ii) the complex signaling interplay that allows cell death signals to be decoded into mitochondria as messages controlling cell fate.
Export Options
About this article
Cite this article as:
Pinton Paolo, Romagnoli Anna, Rizzuto Rosario and Giorgi Carlotta, Ca2+ Signaling, Mitochondria and Cell Death, Current Molecular Medicine 2008; 8 (2) . https://dx.doi.org/10.2174/156652408783769571
DOI https://dx.doi.org/10.2174/156652408783769571 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Impact of Sex Hormone Metabolism on the Vascular Effects of Menopausal Hormone Therapy in Cardiovascular Disease
Current Drug Metabolism Tissue Engineering for Post-Myocardial Infarction Ventricular Remodeling
Mini-Reviews in Medicinal Chemistry Vasoprotective Actions of the Atrial Natriuretic Peptide
Current Medicinal Chemistry - Cardiovascular & Hematological Agents Mitochondria in Chronic Liver Disease
Current Drug Targets Pathogenesis of Acute Kidney Injury During Sepsis
Current Drug Targets Na+/Ca2+ Exchange Inhibitors: A New Class of Calcium Regulators
Cardiovascular & Hematological Disorders-Drug Targets The Role of Adenosine in Rheumatoid Arthritis
Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry (Discontinued) DNA Repair Proteins as Molecular Therapeutics for Oxidative and Alkylating Lung Injury
Current Gene Therapy Atomoxetine Protects Against NMDA Receptor-mediated Hippocampal Neuronal Death Following Transient Global Cerebral Ischemia
Current Neurovascular Research Editorial [Hot Topic (1): Update on Inflammatory Processes Governing Atherosclerotic Plaque Vulnerability and Reperfusion Injury (Guest Editors: Fabrizio Montecucco and Francois Mach)]
Current Pharmaceutical Biotechnology Global Cerebral Ischemia: Synaptic and Cognitive Dysfunction
Current Drug Targets Glycogen Synthase Kinase-3: A Potential Target for Drug Discovery in the Treatment of Neurodegenerative Disorders
Current Enzyme Inhibition Myocardial Energy Transport and Heart Failure
Current Cardiology Reviews Glibenclamide Action on Myocardial Function and Arrhythmia Incidence in the Healthy and Diabetic Heart
Cardiovascular & Hematological Agents in Medicinal Chemistry The Neuroprotective Role of PEDF: Implication for the Therapy of Neurological Disorders
Current Molecular Medicine Editorial (Current and Emerging Pharmacological Therapies of Ischaemic Stroke)
CNS & Neurological Disorders - Drug Targets Mechanisms of the Penetration of Blood-Borne Substances into the Brain
Current Neuropharmacology Advancements within Modern Machine Learning Methodology: Impacts and Prospects in Biomarker Discovery
Current Medicinal Chemistry Small Heat Shock Proteins (sHSPs) As Potential Drug Targets
Current Pharmaceutical Biotechnology "Take and Run" and "Take and Hold" Therapeutical Electromagnetic Field Application Modalities in Physiotherapy: Some Clinically Significant Pathways of Action
Current Chemical Biology