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Chronic obstructive pulmonary disease (COPD) is regarded as a persistent respiratory symptom, mainly caused by cigarette smoking. Recent data have suggested that some miRNAs are involved in the pathogenesis of COPD. Here, we found that miR-195 was significantly upregulated in the lung tissues of patients with COPD compared to in never smokers. miR-195 expression was also upregulated in cigarette smoke (CS)-exposed mice. Lentivirus-mediated knockdown of miR-195 alleviated CS-induced lung pathological changes and reduced inflammatory cell infiltration as well as production of interleukin-6 and tumor necrosis factor-α in bronchoalveolar lavage fluid. Mechanically, a positive correlation was found between miR-195 and phosphorylation of Akt in lung tissues of COPD patients. PHLPP2 was confirmed as a direct downstream target of miR-195 and negative regulator of miR-195 expression. Inhibition of PHLPP2 enhanced Akt phosphorylation and increased interleukin-6 and tumor necrosis factor-α production in BEAS-2B cells, resembling the effects of miR-195 overexpression. Collectively, our data indicate that miR-195 has a pathogenetic role in CS-induced COPD and regulates Akt signaling by suppressing PHLPP2 expression. miR-195 may be an effective therapeutic target in COPD.Expression of miR-195 was increased in peripheral lung tissues from COPD patients.Inhibition of miR-195 relieved CS-induced lung injury and blocked the inflammatory processes in vivo.miR-195 elevated Akt phosphorylation by suppressing PHLPP2 expression.PHLPP2 was involved in miR-195–induced enhancement of Akt phosphorylation and cytokine production.