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[DOI] [PubMed] [Google Scholar] 212.Dejanovic B, et al

Integrating these findings, we propose a tripartite metabolic-immune axis driving DM-associated pulmonary injury

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GH exerts autocrine/paracrine effects by binding to GHR in the same or a neighboring cell surface and initiating JAK2- and SRC-mediated signaling cascades, which decrease pro-apoptotic molecules (Bax and PPAR) and suppress caspase protein activation (Figure 4A)

Review on new horizons of aggregation induced emission: from design to development