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Fibroblast growth factor 21 (FGF21) is a well\u2010established cardioprotective factor. We aimed to study the role of FGF21 in experimentally induced models and clinical affected patients with cardiac damage due to chronic alcohol consumption. We found that circulating FGF21 levels and cardiac FGF21 and \u03b2\u2010klotho protein levels were increased in subjects with chronic alcohol consumption. As an experimental model of ACM, we fed wild\u2010type and Fgf21 knockout (<jats:italic>Fgf21<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup>) mice with a 4% alcohol liquid diet for 4 and 12\u2009weeks. FGF21 circulating levels and FGF21 expression in the myocardium were also increased in wild\u2010type mice after chronic alcohol intake. <jats:italic>Fgf21<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice develop a higher degree of cardiac hypertrophy, fibrosis, and cardiac dysfunction after chronic alcohol consumption than wild\u2010type mice. Moreover, the myocardium of <jats:italic>Fgf21<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice showed signs of metabolic deregulation, oxidative stress, and mitochondrial dysfunction after alcohol intake. Finally, human cardiac biopsies from patients with chronic alcohol consumption developing ACM presented a higher degree of oxidative stress which positively correlated with the FGF21 protein levels in the myocardium. We conclude that plasma levels and cardiac myocyte FGF21 expression were induced in response to chronic alcohol consumption. The lack of FGF21 aggravated cardiac damage produced by ACM, in association with enhanced mitochondrial and oxidative stress, thus pointing to FGF21 as a protective agent against development of alcohol\u2010induced cardiomyopathy. \u00a9 2020 The Pathological Society of Great Britain and Ireland. 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