Causal roles of mitochondrial dynamics in longevity and healthy aging

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Abstract

<p id="d224367e184">Mitochondria are organized in the cell in the form of a dynamic, interconnected network. Mitochondrial dynamics, regulated by mitochondrial fission, fusion, and trafficking, ensure restructuring of this complex reticulum in response to nutrient availability, molecular signals, and cellular stress. Aberrant mitochondrial structures have long been observed in aging and age‐related diseases indicating that mitochondrial dynamics are compromised as cells age. However, the specific mechanisms by which aging affects mitochondrial dynamics and whether these changes are causally or casually associated with cellular and organismal aging is not clear. Here, we review recent studies that show specifically how mitochondrial fission, fusion, and trafficking are altered with age. We discuss factors that change with age to directly or indirectly influence mitochondrial dynamics while examining causal roles for altered mitochondrial dynamics in healthy aging and underlying functional outputs that might affect longevity. Lastly, we propose that altered mitochondrial dynamics might not just be a passive consequence of aging but might constitute an adaptive mechanism to mitigate age‐dependent cellular impairments and might be targeted to increase longevity and promote healthy aging. </p><p class="first" id="d224367e187">Mitochondria form a dynamic, interconnected network that is shaped by fusion, fission and trafficking. This review discusses how aging affects mitochondrial dynamics and how such alterations in turn might help the organism to cope with age‐dependent cellular impairments. <div class="boxed-text panel" id="embr201948395-blkfxd-0001"> <a class="named-anchor" id="embr201948395-blkfxd-0001">  </a> <div class="figure-container so-text-align-c"> <img alt="" class="figure" src="/document_file/dce1a13e-c6f7-4414-9db7-8c8f6e816c41/PubMedCentral/image/EMBR-20-e48395-g005.jpg"/> </div> <div class="panel-content"/> </div> </p>

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Intestinal Short Chain Fatty Acids and their Link with Diet and Human Health

David Ríos-Covián, Patricia Ruas-Madiedo, Abelardo Margolles … (2016)

The colon is inhabited by a dense population of microorganisms, the so-called “gut microbiota,” able to ferment carbohydrates and proteins that escape absorption in the small intestine during digestion. This microbiota produces a wide range of metabolites, including short chain fatty acids (SCFA). These compounds are absorbed in the large bowel and are defined as 1-6 carbon volatile fatty acids which can present straight or branched-chain conformation. Their production is influenced by the pattern of food intake and diet-mediated changes in the gut microbiota. SCFA have distinct physiological effects: they contribute to shaping the gut environment, influence the physiology of the colon, they can be used as energy sources by host cells and the intestinal microbiota and they also participate in different host-signaling mechanisms. We summarize the current knowledge about the production of SCFA, including bacterial cross-feedings interactions, and the biological properties of these metabolites with impact on the human health.

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Kinesin superfamily motor proteins and intracellular transport.

Nobutaka Hirokawa, Yasuko Noda, Yosuke Tanaka … (2009)

Intracellular transport is fundamental for cellular function, survival and morphogenesis. Kinesin superfamily proteins (also known as KIFs) are important molecular motors that directionally transport various cargos, including membranous organelles, protein complexes and mRNAs. The mechanisms by which different kinesins recognize and bind to specific cargos, as well as how kinesins unload cargo and determine the direction of transport, have now been identified. Furthermore, recent molecular genetic experiments have uncovered important and unexpected roles for kinesins in the regulation of such physiological processes as higher brain function, tumour suppression and developmental patterning. These findings open exciting new areas of kinesin research.

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Decline in skeletal muscle mitochondrial function with aging in humans.

Kevin R. Short, Maureen L Bigelow, Jane C. Kahl … (2005)

Cumulative mtDNA damage occurs in aging animals, and mtDNA mutations are reported to accelerate aging in mice. We determined whether aging results in increased DNA oxidative damage and reduced mtDNA abundance and mitochondrial function in skeletal muscle of human subjects. Studies performed in 146 healthy men and women aged 18-89 yr demonstrated that mtDNA and mRNA abundance and mitochondrial ATP production all declined with advancing age. Abundance of mtDNA was positively related to mitochondrial ATP production rate, which in turn, was closely associated with aerobic capacity and glucose tolerance. The content of several mitochondrial proteins was reduced in older muscles, whereas the level of the oxidative DNA lesion, 8-oxo-deoxyguanosine, was increased, supporting the oxidative damage theory of aging. These results demonstrate that age-related muscle mitochondrial dysfunction is related to reduced mtDNA and muscle functional changes that are common in the elderly.