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HLA‐DQA1*05:05:17:03 differs from HLA‐DQA1*05:05:01:02 by a single base substitution in exon 1 and HLA‐DQA1*05:05:17:01 within introns 1 and 2. [ABSTRACT FROM AUTHOR]

HLA‐C*06:372 differs from HLA‐C*06:02:01:01 by a single substitution in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐B*41:84 has a single base substitution in exon 2, altering glutamic acid to glutamine'. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]