ROS production by mitochondria: function or dysfunction?

In eukaryotic cells, ATP generation is generally viewed as the primary function of mitochondria under normoxic conditions. Reactive oxygen species (ROS), in contrast, are regarded as the by-products of respiration, and are widely associated with dysfunction and disease. Important signaling functions...

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Vydané v:Oncogene Ročník 43; číslo 5; s. 295 - 303
Hlavní autori: Palma, Flavio R., Gantner, Benjamin N., Sakiyama, Marcelo J., Kayzuka, Cezar, Shukla, Sanjeev, Lacchini, Riccardo, Cunniff, Brian, Bonini, Marcelo G.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: London Nature Publishing Group UK 29.01.2024
Nature Publishing Group
Predmet:
631/45
631/67/2327
Apoptosis
Cell Biology
Human Genetics
Internal Medicine
Medicine
Medicine & Public Health
Mitochondria
Oncology
Reactive oxygen species
Review Article
ISSN:0950-9232, 1476-5594, 1476-5594
On-line prístup:Získať plný text
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Abstract In eukaryotic cells, ATP generation is generally viewed as the primary function of mitochondria under normoxic conditions. Reactive oxygen species (ROS), in contrast, are regarded as the by-products of respiration, and are widely associated with dysfunction and disease. Important signaling functions have been demonstrated for mitochondrial ROS in recent years. Still, their chemical reactivity and capacity to elicit oxidative damage have reinforced the idea that ROS are the products of dysfunctional mitochondria that accumulate during disease. Several studies support a different model, however, by showing that: (1) limited oxygen availability results in mitochondria prioritizing ROS production over ATP, (2) ROS is an essential adaptive mitochondrial signal triggered by various important stressors, and (3) while mitochondria-independent ATP production can be easily engaged by most cells, there is no known replacement for ROS-driven redox signaling. Based on these observations and other evidence reviewed here, we highlight the role of ROS production as a major mitochondrial function involved in cellular adaptation and stress resistance. As such, we propose a rekindled view of ROS production as a primary mitochondrial function as essential to life as ATP production itself.
AbstractList In eukaryotic cells, ATP generation is generally viewed as the primary function of mitochondria under normoxic conditions. Reactive oxygen species (ROS), in contrast, are regarded as the by-products of respiration, and are widely associated with dysfunction and disease. Important signaling functions have been demonstrated for mitochondrial ROS in recent years. Still, their chemical reactivity and capacity to elicit oxidative damage have reinforced the idea that ROS are the products of dysfunctional mitochondria that accumulate during disease. Several studies support a different model, however, by showing that: (1) limited oxygen availability results in mitochondria prioritizing ROS production over ATP, (2) ROS is an essential adaptive mitochondrial signal triggered by various important stressors, and (3) while mitochondria-independent ATP production can be easily engaged by most cells, there is no known replacement for ROS-driven redox signaling. Based on these observations and other evidence reviewed here, we highlight the role of ROS production as a major mitochondrial function involved in cellular adaptation and stress resistance. As such, we propose a rekindled view of ROS production as a primary mitochondrial function as essential to life as ATP production itself.
In eukaryotic cells, ATP generation is generally viewed as the primary function of mitochondria under normoxic conditions. Reactive oxygen species (ROS), in contrast, are regarded as the by-products of respiration, and are widely associated with dysfunction and disease. Important signaling functions have been demonstrated for mitochondrial ROS in recent years. Still, their chemical reactivity and capacity to elicit oxidative damage have reinforced the idea that ROS are the products of dysfunctional mitochondria that accumulate during disease. Several studies support a different model, however, by showing that: (1) limited oxygen availability results in mitochondria prioritizing ROS production over ATP, (2) ROS is an essential adaptive mitochondrial signal triggered by various important stressors, and (3) while mitochondria-independent ATP production can be easily engaged by most cells, there is no known replacement for ROS-driven redox signaling. Based on these observations and other evidence reviewed here, we highlight the role of ROS production as a major mitochondrial function involved in cellular adaptation and stress resistance. As such, we propose a rekindled view of ROS production as a primary mitochondrial function as essential to life as ATP production itself.In eukaryotic cells, ATP generation is generally viewed as the primary function of mitochondria under normoxic conditions. Reactive oxygen species (ROS), in contrast, are regarded as the by-products of respiration, and are widely associated with dysfunction and disease. Important signaling functions have been demonstrated for mitochondrial ROS in recent years. Still, their chemical reactivity and capacity to elicit oxidative damage have reinforced the idea that ROS are the products of dysfunctional mitochondria that accumulate during disease. Several studies support a different model, however, by showing that: (1) limited oxygen availability results in mitochondria prioritizing ROS production over ATP, (2) ROS is an essential adaptive mitochondrial signal triggered by various important stressors, and (3) while mitochondria-independent ATP production can be easily engaged by most cells, there is no known replacement for ROS-driven redox signaling. Based on these observations and other evidence reviewed here, we highlight the role of ROS production as a major mitochondrial function involved in cellular adaptation and stress resistance. As such, we propose a rekindled view of ROS production as a primary mitochondrial function as essential to life as ATP production itself.
Author Palma, Flavio R.
Bonini, Marcelo G.
Sakiyama, Marcelo J.
Shukla, Sanjeev
Cunniff, Brian
Lacchini, Riccardo
Gantner, Benjamin N.
Kayzuka, Cezar
Author_xml – sequence: 1
  givenname: Flavio R.
  orcidid: 0000-0003-4350-2708
  surname: Palma
  fullname: Palma, Flavio R.
  organization: Department of Medicine, Division of Hematology Oncology, Feinberg School of Medicine and the Robert H. Lurie Comprehensive Cancer Center of Chicago, Northwestern University
– sequence: 2
  givenname: Benjamin N.
  orcidid: 0000-0002-6947-7670
  surname: Gantner
  fullname: Gantner, Benjamin N.
  organization: Department of Medicine, Medical College of Wisconsin
– sequence: 3
  givenname: Marcelo J.
  surname: Sakiyama
  fullname: Sakiyama, Marcelo J.
  organization: Department of Medicine, Division of Hematology Oncology, Feinberg School of Medicine and the Robert H. Lurie Comprehensive Cancer Center of Chicago, Northwestern University
– sequence: 4
  givenname: Cezar
  surname: Kayzuka
  fullname: Kayzuka, Cezar
  organization: Department of Pharmacology, Ribeirao Preto College of Nursing, University of Sao Paulo
– sequence: 5
  givenname: Sanjeev
  orcidid: 0000-0003-3361-0588
  surname: Shukla
  fullname: Shukla, Sanjeev
  organization: Department of Biological Sciences, Indian Institute of Science Education and Research Bhopal
– sequence: 6
  givenname: Riccardo
  surname: Lacchini
  fullname: Lacchini, Riccardo
  organization: Department of Psychiatric Nursing and Human Sciences, Ribeirao Preto College of Nursing, University of Sao Paulo
– sequence: 7
  givenname: Brian
  surname: Cunniff
  fullname: Cunniff, Brian
  organization: Department of Pathology and Laboratory Medicine, Larner School of Medicine, University of Vermont
– sequence: 8
  givenname: Marcelo G.
  orcidid: 0000-0003-1193-1428
  surname: Bonini
  fullname: Bonini, Marcelo G.
  email: Marcelo.bonini@northwestern.edu
  organization: Department of Medicine, Division of Hematology Oncology, Feinberg School of Medicine and the Robert H. Lurie Comprehensive Cancer Center of Chicago, Northwestern University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/38081963$$D View this record in MEDLINE/PubMed
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2023. The Author(s), under exclusive licence to Springer Nature Limited.
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Apoptosis
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Mitochondria
Oncology
Reactive oxygen species
Review Article
Title ROS production by mitochondria: function or dysfunction?
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