The circadian rhythm provides an anticipatory mechanism that allows organisms to adapt to changes in their environment, including their response to external threats such as infections. As an organ exposed constantly to the environment, circadian rhythms are especially important for the lung’s response to infections. Our previous work demonstrated that the circadian clock provides time-of-day protection against influenza A virus (IAV) infection, and genetically disrupting the clock abrogated this time-of-day specific protection. In elucidating the cellular mechanisms, we uncovered a significant role for the clock resident in alveolar type 2 cells, epithelial cells in the most distal airway space that also serve as facultative progenitor cells following injury. Disruption of the AT2 clock impaired post-flu epithelial regeneration, which is essential for recovery. To determine whether this clock also regulates lung regeneration for non-infectious injuries, we treated Sftpc-Cre+ mice with bleomycin. Sftpc-Cre+ mice experienced worsened morbidity and lung injury based on histology compared to their Cre- counterparts, which suggests that the AT2 clock affects both infectious and non-infectious injury models. Wnt-signaling is one of the main signaling pathways that drives optimal lung regeneration after injury, leading to a possible mechanistic association with the AT2 clock. Thus, we also investigated if and how the clock affects Wnt-signaling. To do so, we generated a strain wherein the clock has been disrupted by the deletion of the core clock gene Bmal1 in Wnt-responsive cells in the lungs, marked by Axin2. Following IAV, Axin2-Cre+ mice experienced greater weight loss and mortality rates than their creneg littermates. On histological assessment, there were no significant differences in the immune cell infiltration within peri-bronchial, peri-vascular, or alveolar areas on day 8 post-infection. Through these findings, we thus concluded that the circadian regulation of Wnt-signaling is essential for promoting alveolar regeneration after lung injury without amplifying the immune response. Future work will be necessary to define the molecular mechanisms underlying this.