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The endoplasmic reticulum (<jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content>) plays a pivotal role in protein folding and calcium homeostasis in many mammalian cell types, including skeletal muscle. However, overload of misfolded or unfolded proteins in the <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> lumen cause stress, which results in the activation of a signaling network called the unfolded protein response (<jats:styled-content style=\"fixed-case\">UPR<\/jats:styled-content>). The <jats:styled-content style=\"fixed-case\">UPR<\/jats:styled-content> is initiated by three <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> transmembrane sensors: protein kinase R\u2010like endoplasmic reticulum kinase, inositol\u2010requiring protein 1\u03b1, and activating transcription factor 6. The <jats:styled-content style=\"fixed-case\">UPR<\/jats:styled-content> restores <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> homeostasis through modulating the rate of protein synthesis and augmenting the gene expression of many <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> chaperones and regulatory proteins. However, chronic heightened <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> stress can also lead to many pathological consequences including cell death. Accumulating evidence suggests that <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> stress\u2010induced <jats:styled-content style=\"fixed-case\">UPR<\/jats:styled-content> pathways play pivotal roles in the regulation of skeletal muscle mass and metabolic function in multiple conditions. They have also been found to be activated in skeletal muscle under catabolic states, degenerative muscle disorders, and various types of myopathies. In this article, we have discussed the recent advancements toward understanding the role and mechanisms through which <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content> stress and individual arms of the <jats:styled-content style=\"fixed-case\">UPR<\/jats:styled-content> regulate skeletal muscle physiology and pathology.<\/jats:p>","DOI":"10.1111\/febs.14358","type":"journal-article","created":{"date-parts":[[2017,12,14]],"date-time":"2017-12-14T09:42:37Z","timestamp":1513244557000},"page":"379-398","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":156,"title":["<scp>ER<\/scp> stress in skeletal muscle remodeling and myopathies"],"prefix":"10.1111","volume":"286","author":[{"given":"Dil","family":"Afroze","sequence":"first","affiliation":[{"name":"Department of Anatomical Sciences and Neurobiology University of Louisville School of Medicine KY USA"},{"name":"Department of Immunology and Molecular Medicine 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