2017
DOI: 10.18632/aging.101213
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Abstract: Decreased energy production and increased oxidative stress are considered to be major contributors to aging and aging-associated pathologies. The role of mitochondrial calcium homeostasis has also been highlighted as an important factor affecting different pathological conditions. Here, we present evidence that loss of a small mitochondrial protein Fus1 that maintains mitochondrial homeostasis results in premature aging, aging-associated pathologies, and decreased survival. We showed that Fus1KO mice develop m… Show more

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Cited by 16 publications
(30 citation statements)
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References 113 publications
(126 reference statements)
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“…Aging is complex set of genetic [40,41], epigenetic [4246], immunological [4751], and metabolic [5258] rearrangements, involving several cellular signalling pathways [5963] able to regulate metabolism, ROS formation [6471] and DNA Damage Response (DDR) [7274] in all organs [7577]. Therefore, the identification of novel pathways involving p53-mediated responses [78,79] is of crucial interest.…”
Section: Discussionmentioning
confidence: 99%
“…E.g. Fis1 KO mice develop multiple early aging signs including lordokyphosis, lack of vigor, inability to accumulate fat, reduced ability to tolerate stress, perturbed Ca 2+ dynamics, and decreased lifespan (Uzhachenko et al, 2017). Transmembrane protein 135 (TMEM135) is a protein likely involved in mitochondrial fission and mice with mutated TMEM135 display abnormal mitochondrial dynamics and accelerated aging in the retina as well as pathologies observed in agedependent retinal diseases (Lee et al, 2016b).…”
Section: Drosophila Model Shows Opposite Trend Upregulating Drp1 Expmentioning
confidence: 99%
“…The importance of sufficient mitochondrial Ca 2+ uptake was demonstrated in mice lacking Fus1, a small mitochondrial protein regulating mitochondrial Ca 2+ homeostasis. Loss of Fus1 caused inefficient accumulation of Ca 2+ in mitochondria and decreased respiratory reserve capacity, resulting in the decreased lifespan of mice with knockout of Fus1 [ 74 ]. These partly conflicting results suggest that fine-tuning of mitochondrial Ca 2+ homeostasis during aging is a tightrope walk between meeting mitochondria’s demand for Ca 2+ [ 74 ] and triggering harmful processes like increased ROS production or mPTP opening by Ca 2+ overload [ 74 ].…”
Section: Mitochondrial Changes During Agingmentioning
confidence: 99%
“…The mechanisms behind inflammageing have not been fully elucidated yet. Despite this, we believe that the mechanisms are complex and closely associated with genetic and epigenetic factors [8] , mitochondrial dysfunction [9] , [10] , and small metabolic and homoeostatic dysregulations leading to a maladaptation to normal stresses, thus resulting in macromolecular/cell/tissue damage. In this way, chronic low-grade inflammation could contribute to many ageing-associated orthopaedic and rheumatological pathologies such as osteoporosis [11] , osteoarthritis [12] , and sarcopaenia [13] .…”
Section: Current Concept Of Inflammatory Mechanismsmentioning
confidence: 99%
“…Among these, oxidative stress is perhaps the most fundamental cause of age-related pathology in the biological aging of cells and may be an important intrinsic factor in presbycusis. Oxidative stress is caused by accumulation of mitochondrial DNA mutations and/or deletions (or reduced mitochondrial DNA gene expression), leading to a mitochondrial dysfunction in maintain the homeostatic level of free radicals [9] [14]. Falah et al found a total of 113 sequence variants in mitochondrial DNA in 100% of their presbycusis patients and supported the idea of the role of mitochondria in the intracellular mechanism underlying presbycusis development.…”
Section: Introductionmentioning
confidence: 99%