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The stress response is coupled to EMT<\/jats:styled-content> and kidney injury; however, the underlying mechanism of the stress response in EMT<\/jats:styled-content> remains elusive. AMP<\/jats:styled-content>\u2010activated protein kinase (AMPK<\/jats:styled-content>) signalling is responsive to stress and regulates cell energy balance and differentiation. We found that knockdown of AMPK\u03b1<\/jats:styled-content>, especially AMPK\u03b12<\/jats:styled-content>, enhanced EMT<\/jats:styled-content> by up\u2010regulating \u03b2\u2010catenin and Smad3 in vitro<\/jats:italic>. AMPK\u03b12<\/jats:styled-content> deficiency enhanced EMT<\/jats:styled-content> and fibrosis in a murine unilateral ureteral obstruction (UUO<\/jats:styled-content>) model. AMPK\u03b12<\/jats:styled-content> deficiency also increased the expression of chemokines KC<\/jats:styled-content> and MCP<\/jats:styled-content>\u20101, along with enhanced infiltration of inflammatory cells into the kidney after UUO<\/jats:styled-content>. CK2\u03b2<\/jats:styled-content> interacted physically with AMPK\u03b1<\/jats:styled-content> and enhanced AMPK\u03b1<\/jats:styled-content> Thr172 phosphorylation and its catalytic activity. Thus, activated AMPK\u03b1<\/jats:styled-content> signalling suppresses EMT<\/jats:styled-content> and secretion of chemokines in renal tubular epithelia through interaction with CK2\u03b2<\/jats:styled-content> to attenuate renal injury. Copyright \u00a9 2015 Pathological Society of Great Britain and Ireland. 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