Mitochondrial Dysfunction: A Basic Mechanism in Inflammation-Related Non-Communicable Diseases and Therapeutic Opportunities
Obesity is not necessarily a predisposing factor for disease. It is the handling of fat and/or excessive energy intake that encompasses the linkage of inflammation, oxidation, and metabolism to the deleterious effects associated with the continuous excess of food ingestion. The roles of cytokines an...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2013/135698 |
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| author | Anna Hernández-Aguilera Anna Rull Esther Rodríguez-Gallego Marta Riera-Borrull Fedra Luciano-Mateo Jordi Camps Javier A. Menéndez Jorge Joven |
| author_facet | Anna Hernández-Aguilera Anna Rull Esther Rodríguez-Gallego Marta Riera-Borrull Fedra Luciano-Mateo Jordi Camps Javier A. Menéndez Jorge Joven |
| author_sort | Anna Hernández-Aguilera |
| collection | DOAJ |
| description | Obesity is not necessarily a predisposing factor for disease. It is the handling of fat and/or excessive energy intake that encompasses the linkage of inflammation, oxidation, and metabolism to the deleterious effects associated with the continuous excess of food ingestion. The roles of cytokines and insulin resistance in excessive energy intake have been studied extensively. Tobacco use and obesity accompanied by an unhealthy diet and physical inactivity are the main factors that underlie noncommunicable diseases. The implication is that the management of energy or food intake, which is the main role of mitochondria, is involved in the most common diseases. In this study, we highlight the importance of mitochondrial dysfunction in the mutual relationships between causative conditions. Mitochondria are highly dynamic organelles that fuse and divide in response to environmental stimuli, developmental status, and energy requirements. These organelles act to supply the cell with ATP and to synthesise key molecules in the processes of inflammation, oxidation, and metabolism. Therefore, energy sensors and management effectors are determinants in the course and development of diseases. Regulating mitochondrial function may require a multifaceted approach that includes drugs and plant-derived phenolic compounds with antioxidant and anti-inflammatory activities that improve mitochondrial biogenesis and act to modulate the AMPK/mTOR pathway. |
| format | Article |
| id | doaj-art-1f090301a4f7462baf413763c449b6f5 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-1f090301a4f7462baf413763c449b6f52025-02-03T05:57:47ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/135698135698Mitochondrial Dysfunction: A Basic Mechanism in Inflammation-Related Non-Communicable Diseases and Therapeutic OpportunitiesAnna Hernández-Aguilera0Anna Rull1Esther Rodríguez-Gallego2Marta Riera-Borrull3Fedra Luciano-Mateo4Jordi Camps5Javier A. Menéndez6Jorge Joven7Unitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, carrer Sant Llorenç 21, 43201 Reus, SpainUnitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, carrer Sant Llorenç 21, 43201 Reus, SpainUnitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, carrer Sant Llorenç 21, 43201 Reus, SpainUnitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, carrer Sant Llorenç 21, 43201 Reus, SpainUnitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, carrer Sant Llorenç 21, 43201 Reus, SpainUnitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, carrer Sant Llorenç 21, 43201 Reus, SpainCatalan Institute of Oncology and Girona Biomedical Research Institute, Avda de Francia s/n, 1707 Girona, SpainUnitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, carrer Sant Llorenç 21, 43201 Reus, SpainObesity is not necessarily a predisposing factor for disease. It is the handling of fat and/or excessive energy intake that encompasses the linkage of inflammation, oxidation, and metabolism to the deleterious effects associated with the continuous excess of food ingestion. The roles of cytokines and insulin resistance in excessive energy intake have been studied extensively. Tobacco use and obesity accompanied by an unhealthy diet and physical inactivity are the main factors that underlie noncommunicable diseases. The implication is that the management of energy or food intake, which is the main role of mitochondria, is involved in the most common diseases. In this study, we highlight the importance of mitochondrial dysfunction in the mutual relationships between causative conditions. Mitochondria are highly dynamic organelles that fuse and divide in response to environmental stimuli, developmental status, and energy requirements. These organelles act to supply the cell with ATP and to synthesise key molecules in the processes of inflammation, oxidation, and metabolism. Therefore, energy sensors and management effectors are determinants in the course and development of diseases. Regulating mitochondrial function may require a multifaceted approach that includes drugs and plant-derived phenolic compounds with antioxidant and anti-inflammatory activities that improve mitochondrial biogenesis and act to modulate the AMPK/mTOR pathway.http://dx.doi.org/10.1155/2013/135698 |
| spellingShingle | Anna Hernández-Aguilera Anna Rull Esther Rodríguez-Gallego Marta Riera-Borrull Fedra Luciano-Mateo Jordi Camps Javier A. Menéndez Jorge Joven Mitochondrial Dysfunction: A Basic Mechanism in Inflammation-Related Non-Communicable Diseases and Therapeutic Opportunities Mediators of Inflammation |
| title | Mitochondrial Dysfunction: A Basic Mechanism in Inflammation-Related Non-Communicable Diseases and Therapeutic Opportunities |
| title_full | Mitochondrial Dysfunction: A Basic Mechanism in Inflammation-Related Non-Communicable Diseases and Therapeutic Opportunities |
| title_fullStr | Mitochondrial Dysfunction: A Basic Mechanism in Inflammation-Related Non-Communicable Diseases and Therapeutic Opportunities |
| title_full_unstemmed | Mitochondrial Dysfunction: A Basic Mechanism in Inflammation-Related Non-Communicable Diseases and Therapeutic Opportunities |
| title_short | Mitochondrial Dysfunction: A Basic Mechanism in Inflammation-Related Non-Communicable Diseases and Therapeutic Opportunities |
| title_sort | mitochondrial dysfunction a basic mechanism in inflammation related non communicable diseases and therapeutic opportunities |
| url | http://dx.doi.org/10.1155/2013/135698 |
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