Electron Transport

Publication Title: 
Biochimica Et Biophysica Acta

Ageing can be defined as "a progressive, generalized impairment of function, resulting in an increased vulnerability to environmental challenge and a growing risk of disease and death". Ageing is likely a multifactorial process caused by accumulated damage to a variety of cellular components. During the last 20 years, gerontological studies have revealed different molecular pathways involved in the ageing process and pointed out mitochondria as one of the key regulators of longevity.

Author(s): 
Bratic, Ivana
Trifunovic, Aleksandra
Publication Title: 
PLoS biology

An increasing number of genes required for mitochondrial biogenesis, dynamics, or function have been found to be mutated in metabolic disorders and neurological diseases such as Leigh Syndrome. In a forward genetic screen to identify genes required for neuronal function and survival in Drosophila photoreceptor neurons, we have identified mutations in the mitochondrial methionyl-tRNA synthetase, Aats-met, the homologue of human MARS2. The fly mutants exhibit age-dependent degeneration of photoreceptors, shortened lifespan, and reduced cell proliferation in epithelial tissues.

Author(s): 
Bayat, Vafa
Thiffault, Isabelle
Jaiswal, Manish
TÈtreault, Martine
Donti, Taraka
Sasarman, Florin
Bernard, GeneviËve
Demers-Lamarche, Julie
Dicaire, Marie-JosÈe
Mathieu, Jean
Vanasse, Michel
Bouchard, Jean-Pierre
Rioux, Marie-France
Lourenco, Charles M.
Li, Zhihong
Haueter, Claire
Shoubridge, Eric A.
Graham, Brett H.
Brais, Bernard
Bellen, Hugo J.
Publication Title: 
Human Molecular Genetics

The CISD2 gene, which is an evolutionarily conserved novel gene, encodes a transmembrane protein primarily associated with the mitochondrial outer membrane. Significantly, the CISD2 gene is located within the candidate region on chromosome 4q where a genetic component for human longevity has been mapped. Previously, we have shown that Cisd2 deficiency shortens lifespan resulting in premature aging in mice. Additionally, an age-dependent decrease in Cisd2 expression has been detected during normal aging.

Author(s): 
Wu, Chia-Yu
Chen, Yi-Fan
Wang, Chih-Hao
Kao, Cheng-Heng
Zhuang, Hui-Wen
Chen, Chih-Cheng
Chen, Liang-Kung
Kirby, Ralph
Wei, Yau-Huei
Tsai, Shih-Feng
Tsai, Ting-Fen
Publication Title: 
Cellular and molecular life sciences: CMLS

Reduction of nutrient intake without malnutrition positively influences lifespan and healthspan from yeast to mice and exerts some beneficial effects also in humans. The AMPK-FoxO axis is one of the evolutionarily conserved nutrient-sensing pathways, and the FOXO3A locus is associated with human longevity. Interestingly, FoxO3A has been reported to be also a mitochondrial protein in mammalian cells and tissues. Here we report that glucose restriction triggers FoxO3A accumulation into mitochondria of fibroblasts and skeletal myotubes in an AMPK-dependent manner.

Author(s): 
Peserico, Alessia
Chiacchiera, Fulvio
Grossi, Valentina
Matrone, Antonio
Latorre, Dominga
Simonatto, Marta
Fusella, Aurora
Ryall, James G.
Finley, Lydia W. S.
Haigis, Marcia C.
Villani, Gaetano
Puri, Pier Lorenzo
Sartorelli, Vittorio
Simone, Cristiano
Publication Title: 
The Journal of Nutrition, Health & Aging

The hypothesis that the generation of reactive oxygen species (ROS) is the principal mechanism responsible for ageing, is reviewed in relation to the influence of diet and dietary factors on the generation of ROS and the effects on life span. Particular focus has been placed on the generation of ROS in the mitochondria, the effects this has on oxidative damage to cellular macromolecules, and the evidence that dietary factors can reduce this damage.

Author(s): 
Lindsay, D. G.
Publication Title: 
Cell Metabolism

Age-related disease, not aging per se, causes most morbidity in older humans. Here we report that skeletal muscle respiratory uncoupling due to UCP1 expression diminishes age-related disease in three mouse models. In a longevity study, median survival was increased in UCP mice (animals with skeletal muscle-specific UCP1 expression), and lymphoma was detected less frequently in UCP female mice. In apoE null mice, a vascular disease model, diet-induced atherosclerosis was decreased in UCP animals.

Author(s): 
Gates, Allison C.
Bernal-Mizrachi, Carlos
Chinault, Sharon L.
Feng, Chu
Schneider, Jochen G.
Coleman, Trey
Malone, James P.
Townsend, R. Reid
Chakravarthy, Manu V.
Semenkovich, Clay F.
Publication Title: 
Biochimica Et Biophysica Acta

Ageing can be defined as "a progressive, generalized impairment of function, resulting in an increased vulnerability to environmental challenge and a growing risk of disease and death". Ageing is likely a multifactorial process caused by accumulated damage to a variety of cellular components. During the last 20 years, gerontological studies have revealed different molecular pathways involved in the ageing process and pointed out mitochondria as one of the key regulators of longevity.

Author(s): 
Bratic, Ivana
Trifunovic, Aleksandra
Publication Title: 
Nature Communications

Metformin is a drug commonly prescribed to treat patients with type 2 diabetes. Here we show that long-term treatment with metformin (0.1% w/w in diet) starting at middle age extends healthspan and lifespan in male mice, while a higher dose (1% w/w) was toxic. Treatment with metformin mimics some of the benefits of calorie restriction, such as improved physical performance, increased insulin sensitivity, and reduced low-density lipoprotein and cholesterol levels without a decrease in caloric intake.

Author(s): 
Martin-Montalvo, Alejandro
Mercken, Evi M.
Mitchell, Sarah J.
Palacios, Hector H.
Mote, Patricia L.
Scheibye-Knudsen, Morten
Gomes, Ana P.
Ward, Theresa M.
Minor, Robin K.
Blouin, Marie-José
Schwab, Matthias
Pollak, Michael
Zhang, Yongqing
Yu, Yinbing
Becker, Kevin G.
Bohr, Vilhelm A.
Ingram, Donald K.
Sinclair, David A.
Wolf, Norman S.
Spindler, Stephen R.
Bernier, Michel
de Cabo, Rafael
Publication Title: 
PLoS genetics

Artemisinins, derived from the wormwood herb Artemisia annua, are the most potent antimalarial drugs currently available. Despite extensive research, the exact mode of action of artemisinins has not been established. Here we use yeast, Saccharamyces cerevisiae, to probe the core working mechanism of this class of antimalarial agents. We demonstrate that artemisinin's inhibitory effect is mediated by disrupting the normal function of mitochondria through depolarizing their membrane potential.

Author(s): 
Li, Wei
Mo, Weike
Shen, Dan
Sun, Libo
Wang, Juan
Lu, Shan
Gitschier, Jane M.
Zhou, Bing
Publication Title: 
Proceedings of the National Academy of Sciences of the United States of America

There is an urgent need for new antimalarial drugs with novel mechanisms of action to deliver effective control and eradication programs. Parasite resistance to all existing antimalarial classes, including the artemisinins, has been reported during their clinical use. A failure to generate new antimalarials with novel mechanisms of action that circumvent the current resistance challenges will contribute to a resurgence in the disease which would represent a global health emergency.

Author(s): 
Biagini, Giancarlo A.
Fisher, Nicholas
Shone, Alison E.
Mubaraki, Murad A.
Srivastava, Abhishek
Hill, Alisdair
Antoine, Thomas
Warman, Ashley J.
Davies, Jill
Pidathala, Chandrakala
Amewu, Richard K.
Leung, Suet C.
Sharma, Raman
Gibbons, Peter
Hong, David W.
Pacorel, Bénédicte
Lawrenson, Alexandre S.
Charoensutthivarakul, Sitthivut
Taylor, Lee
Berger, Olivier
Mbekeani, Alison
Stocks, Paul A.
Nixon, Gemma L.
Chadwick, James
Hemingway, Janet
Delves, Michael J.
Sinden, Robert E.
Zeeman, Anne-Marie
Kocken, Clemens H. M.
Berry, Neil G.
O'Neill, Paul M.
Ward, Stephen A.

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