Mitochondrial dysfunctions related with oxidative stress

Alfredo Saavedra-Molina, Istvan Boldogh, Salvador Manzo-Avalos, Christian Cortés-Rojo, Leopoldo Aguilera-Aguirre, Rocío Montoya-Pérez, Attila Bacsi

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Mitochondria are central to ATP synthesis, regulation of Ca2+ homeostasis generation of reactive oxygen species and programmed cell death. They have an essential role in the generation of cell activation signals via released reactive species, as well as small GTPases; mitogen activated kinases located in the outer and inner membranes of mitochondria. While mutations of mitochondrial DNA leading to synthesis of malfunctional proteins are the most understood cause of cellular/organelle pathological changes, the mitochondrial dysfunction induced via oxidative damage to DNA, electron transport chain and structural proteins are also etiologically important events in development and progression in a wide array of diseases including malignancies, diabetes, hypertension, inflammation, hepatitis, neuromuscular and neurodegenerative ones. Although there is a growing amount of data regarding the mechanisms of mitochondrial dysfunction, one of the main challenges in the years to come will be to assess whether functional/structural modulation to mitochondrial proteins and damage to DNA is a cause or a consequence of disease. When mechanistic issues are sorted out, the use of mitochondria as a pharmacological target holds unforeseen promise in the treatment of diseases. Here we provide a short overview on newest discoveries supporting implication of mitochondria in inflammatory and apoptosis-based diseases.

Original languageEnglish (US)
Title of host publicationMitochondria: Structure, Functions and Dysfunctions
PublisherNova Science Publishers, Inc.
Pages411-439
Number of pages29
ISBN (Print)9781616683467
StatePublished - 2011

Fingerprint

Mitochondria
Oxidative stress
Oxidative Stress
DNA Damage
Monomeric GTP-Binding Proteins
Mitochondrial Proteins
DNA
Cell death
Medical problems
Electron Transport
Mitochondrial DNA
Mitogens
Organelles
Hepatitis
Reactive Oxygen Species
Proteins
Homeostasis
Cell Death
Phosphotransferases
Adenosine Triphosphate

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Saavedra-Molina, A., Boldogh, I., Manzo-Avalos, S., Cortés-Rojo, C., Aguilera-Aguirre, L., Montoya-Pérez, R., & Bacsi, A. (2011). Mitochondrial dysfunctions related with oxidative stress. In Mitochondria: Structure, Functions and Dysfunctions (pp. 411-439). Nova Science Publishers, Inc..

Mitochondrial dysfunctions related with oxidative stress. / Saavedra-Molina, Alfredo; Boldogh, Istvan; Manzo-Avalos, Salvador; Cortés-Rojo, Christian; Aguilera-Aguirre, Leopoldo; Montoya-Pérez, Rocío; Bacsi, Attila.

Mitochondria: Structure, Functions and Dysfunctions. Nova Science Publishers, Inc., 2011. p. 411-439.

Research output: Chapter in Book/Report/Conference proceedingChapter

Saavedra-Molina, A, Boldogh, I, Manzo-Avalos, S, Cortés-Rojo, C, Aguilera-Aguirre, L, Montoya-Pérez, R & Bacsi, A 2011, Mitochondrial dysfunctions related with oxidative stress. in Mitochondria: Structure, Functions and Dysfunctions. Nova Science Publishers, Inc., pp. 411-439.
Saavedra-Molina A, Boldogh I, Manzo-Avalos S, Cortés-Rojo C, Aguilera-Aguirre L, Montoya-Pérez R et al. Mitochondrial dysfunctions related with oxidative stress. In Mitochondria: Structure, Functions and Dysfunctions. Nova Science Publishers, Inc. 2011. p. 411-439
Saavedra-Molina, Alfredo ; Boldogh, Istvan ; Manzo-Avalos, Salvador ; Cortés-Rojo, Christian ; Aguilera-Aguirre, Leopoldo ; Montoya-Pérez, Rocío ; Bacsi, Attila. / Mitochondrial dysfunctions related with oxidative stress. Mitochondria: Structure, Functions and Dysfunctions. Nova Science Publishers, Inc., 2011. pp. 411-439
@inbook{4092cd6507624479b8f4b1d3a640d96b,
title = "Mitochondrial dysfunctions related with oxidative stress",
abstract = "Mitochondria are central to ATP synthesis, regulation of Ca2+ homeostasis generation of reactive oxygen species and programmed cell death. They have an essential role in the generation of cell activation signals via released reactive species, as well as small GTPases; mitogen activated kinases located in the outer and inner membranes of mitochondria. While mutations of mitochondrial DNA leading to synthesis of malfunctional proteins are the most understood cause of cellular/organelle pathological changes, the mitochondrial dysfunction induced via oxidative damage to DNA, electron transport chain and structural proteins are also etiologically important events in development and progression in a wide array of diseases including malignancies, diabetes, hypertension, inflammation, hepatitis, neuromuscular and neurodegenerative ones. Although there is a growing amount of data regarding the mechanisms of mitochondrial dysfunction, one of the main challenges in the years to come will be to assess whether functional/structural modulation to mitochondrial proteins and damage to DNA is a cause or a consequence of disease. When mechanistic issues are sorted out, the use of mitochondria as a pharmacological target holds unforeseen promise in the treatment of diseases. Here we provide a short overview on newest discoveries supporting implication of mitochondria in inflammatory and apoptosis-based diseases.",
author = "Alfredo Saavedra-Molina and Istvan Boldogh and Salvador Manzo-Avalos and Christian Cort{\'e}s-Rojo and Leopoldo Aguilera-Aguirre and Roc{\'i}o Montoya-P{\'e}rez and Attila Bacsi",
year = "2011",
language = "English (US)",
isbn = "9781616683467",
pages = "411--439",
booktitle = "Mitochondria: Structure, Functions and Dysfunctions",
publisher = "Nova Science Publishers, Inc.",

}

TY - CHAP

T1 - Mitochondrial dysfunctions related with oxidative stress

AU - Saavedra-Molina, Alfredo

AU - Boldogh, Istvan

AU - Manzo-Avalos, Salvador

AU - Cortés-Rojo, Christian

AU - Aguilera-Aguirre, Leopoldo

AU - Montoya-Pérez, Rocío

AU - Bacsi, Attila

PY - 2011

Y1 - 2011

N2 - Mitochondria are central to ATP synthesis, regulation of Ca2+ homeostasis generation of reactive oxygen species and programmed cell death. They have an essential role in the generation of cell activation signals via released reactive species, as well as small GTPases; mitogen activated kinases located in the outer and inner membranes of mitochondria. While mutations of mitochondrial DNA leading to synthesis of malfunctional proteins are the most understood cause of cellular/organelle pathological changes, the mitochondrial dysfunction induced via oxidative damage to DNA, electron transport chain and structural proteins are also etiologically important events in development and progression in a wide array of diseases including malignancies, diabetes, hypertension, inflammation, hepatitis, neuromuscular and neurodegenerative ones. Although there is a growing amount of data regarding the mechanisms of mitochondrial dysfunction, one of the main challenges in the years to come will be to assess whether functional/structural modulation to mitochondrial proteins and damage to DNA is a cause or a consequence of disease. When mechanistic issues are sorted out, the use of mitochondria as a pharmacological target holds unforeseen promise in the treatment of diseases. Here we provide a short overview on newest discoveries supporting implication of mitochondria in inflammatory and apoptosis-based diseases.

AB - Mitochondria are central to ATP synthesis, regulation of Ca2+ homeostasis generation of reactive oxygen species and programmed cell death. They have an essential role in the generation of cell activation signals via released reactive species, as well as small GTPases; mitogen activated kinases located in the outer and inner membranes of mitochondria. While mutations of mitochondrial DNA leading to synthesis of malfunctional proteins are the most understood cause of cellular/organelle pathological changes, the mitochondrial dysfunction induced via oxidative damage to DNA, electron transport chain and structural proteins are also etiologically important events in development and progression in a wide array of diseases including malignancies, diabetes, hypertension, inflammation, hepatitis, neuromuscular and neurodegenerative ones. Although there is a growing amount of data regarding the mechanisms of mitochondrial dysfunction, one of the main challenges in the years to come will be to assess whether functional/structural modulation to mitochondrial proteins and damage to DNA is a cause or a consequence of disease. When mechanistic issues are sorted out, the use of mitochondria as a pharmacological target holds unforeseen promise in the treatment of diseases. Here we provide a short overview on newest discoveries supporting implication of mitochondria in inflammatory and apoptosis-based diseases.

UR - http://www.scopus.com/inward/record.url?scp=84895353142&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84895353142&partnerID=8YFLogxK

M3 - Chapter

AN - SCOPUS:84895353142

SN - 9781616683467

SP - 411

EP - 439

BT - Mitochondria: Structure, Functions and Dysfunctions

PB - Nova Science Publishers, Inc.

ER -