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Early gain\u2010 and loss\u2010of\u2010function studies led to the conclusion that all members of the <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101 family (<jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101\u03b1, <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101\u03b2 and <jats:styled-content style=\"fixed-case\">PRC<\/jats:styled-content>) play redundant roles in the control of mitochondrial biogenesis by regulating overlapping gene expression programs. Regardless of this, all <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101 coactivators also appeared to differ in the stimuli to which they respond to promote mitochondrial gene expression. Although <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101\u03b1 was found to be induced by different physiological or pharmacological cues, <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101\u03b2 appeared to be unresponsive to such stimuli. Consequently, it has long been widely accepted that <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101\u03b1 acts as a mediator of mitochondrial biogenesis induced by cues that signal high\u2010energy needs, whereas the role of <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101\u03b2 is restricted to the maintenance of basal mitochondrial function. By contrast, the function of <jats:styled-content style=\"fixed-case\">PRC<\/jats:styled-content> appears to be restricted to the regulation of gene expression in proliferating cells. However, recent studies using tissue\u2010specific mouse models that lack or overexpress different <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101 coactivators have provided emerging evidence not only supporting new roles for <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101s, but also redefining some of the paradigms related to the precise function and mode of action of <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101 coactivators in mitochondrial biogenesis. The present review discusses some of the new findings regarding the control of mitochondrial gene expression by <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101 coactivators in a tissue\u2010specific context, as well as newly\u2010uncovered functions of <jats:styled-content style=\"fixed-case\">PGC<\/jats:styled-content>\u20101s beyond mitochondrial biogenesis, and their link to pathologies, such as diabetes, muscular dystrophies, neurodegenerative diseases or cancer.<\/jats:p>","DOI":"10.1111\/febs.13175","type":"journal-article","created":{"date-parts":[[2014,12,13]],"date-time":"2014-12-13T13:53:17Z","timestamp":1418478797000},"page":"647-672","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":372,"title":["New insights into <scp>PGC<\/scp>\u20101 coactivators: redefining their role in the regulation of mitochondrial function and beyond"],"prefix":"10.1111","volume":"282","author":[{"given":"Josep 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