Over the past decade, accumulating evidence has suggested a causative link between mitochondrial dysfunction and major phenotypes associated with aging and associated metabolic diseases. Somatic mitochondrial DNA (mtDNA) mutations and respiratory chain dysfunction accompany normal aging. Recent evidence suggests that increases in aging-associated mtDNA mutations are not caused by damage accumulation but rather are due to clonal expansion of mtDNA replication errors that occur during development. Recently, it has become evident that mitochondrial dysfunction is closely related to insulin resistance and metabolic syndrome. The underlying mechanisms of mitochondrial dysfunction are very complex, which includes genetic factors from both nuclear and mitochondrial genome and numerous environmental factors.
The editors of AJP - E&M encourage submissions of novel data highlighting novel mechanisms of actions related to mitochondrial dysfunction in aging and metabolic diseases and how such findings may unravel novel therapeutic targets. We will consider both original research articles and review articles. For review articles only, authors should email the editorial office (email@example.com) with a pre-submission inquiry including a working title, author and affiliation list, abstract, and brief outline of the content for approval by the editors.
Submission Deadline: September 30, 2017