Mechanisms of autophagy regulation by adiponectin

Adiponectin is a multifunctional adipocytokine produced predominantly by adipocytes, with potent antiinflammatory, insulin-sensitizing, and cytoprotective properties. Autophagy is a lysosome-dependent self-degradative process that mediates the degradation of damaged organelles, invading pathogens and protein aggregates, thus maintaining cellular homeostasis. Adiponectin performs different biological functions by regulating autophagy. This review attempts to elucidate the biological responses and potential mechanisms underlying adiponectin-induced autophagy, with an aim to guide the identification of new therapeutic targets of related diseases. Keywords: Adiponectin, adiponectin receptors, autophagy

Improving the Inhibition of TMPRSS2 by Molecular Docking, to Decrease the Process Infection of SARS-CoV-2

COVID-19 pandemic continues with several works focused on the repositioning of drugs, vaccines, and antibodies against COVID-19, as well as new therapeutic targets on the cellular membrane (ACE2, NRP1, and TMPRSS2) that interacting with SARS-CoV-2 S-protein. This study proposes ten compounds (T1 - T10) selected by molecular docking using a library of nearly 500,000 compounds, these ten compounds have better interaction than Daclatasvir, Ombitasvir, Camostat, Edoxaban, NCGC00386477, Nafamostat, NCGC00386945, Otamixaban, Darexaban, Gabexate, Letaxaban, Argatroban, Sivelestat, NCGC00385043, and Bromhexine, and all of them have an inhibitory effect reported at TMPRSS2. The T1 - T10 compounds were selected by molecular docking in the catalytic site of TMPRSS2, which could hinder/block the interaction with the S-protein and ACE2. Therefore the initial/early stage of COVID-19 could be avoided or decreased by hindering the fusion between SARS-CoV-2 and the cell membrane and this way to develop a new adjuvant treatment against COVID-19.