Role of autophagy in cancer-associated fibroblast activation, signaling and metabolic reprograming.

Tumors not only consist of cancerous cells, but they also harbor several normal-like cell types and non-cellular components. cancer-associated fibroblasts (CAFs) are one of these cellular components that are found predominantly in the tumor stroma. Autophagy is an intracellular degradation and quality control mechanism, and recent studies provided evidence that autophagy played a critical role in CAF formation, metabolic reprograming and tumor-stroma crosstalk.

The impact of government pandemic policies on the vulnerability of healthcare workers to SARS-CoV-2 infection and mortality in Jakarta Province, Indonesia.

Introduction: Healthcare workers (HCWs) are on the frontlines of the COVID-19 pandemic, putting them at a higher risk of infection and disease than non-HCWs. We analysed the effects of government policies for the public and for HCWs on the likelihood of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection and mortality among HCWs during the first 8 months of the pandemic in Jakarta province, the capital city and COVID-19 hotspot in Indonesia.

Methods: We conducted a retrospective cohort study using secondary data from the Jakarta provincial government from March to October 2020, which included sociodemographic characteristics, symptoms, comorbidities and COVID-19 diagnosis history for all cases.

Cholesterol accumulation in hepatocytes mediates IRE1/p38 branch of endoplasmic reticulum stress to promote nonalcoholic steatohepatitis.

Non-alcoholic fatty liver disease (NAFLD), based on the elevating obesity incidence, is one of the major health issue worldwide. Transition from NAFLD to non-alcoholic steatohepatitis (NASH) is driven by increased apoptosis and is relevant to higher morbidity rates. In regard to limited understanding on cholesterol mediated hepatocyte alterations in NALFD/NASH transition, we investigated endoplasmic reticulum (ER) stress and related apoptosis.

Deficiency of SREBP1c modulates autophagy mediated lipid droplet catabolism during oleic acid induced steatosis.

Objective: Increased fatty acid and triglyceride synthesis in liver, majorly modulated by Sterol Regulator Elementing Binding Protein 1c (SREBP1c), is one of the main features of non-alcoholic fatty liver disease (NAFLD). In the present study, we aimed to identify the relation between SREBP1c and autophagy mediated lipid droplet (LD) catabolism in oleic acid (OA) induced lipid accumulation.

Methods: Increased LD formation and SREBP1c induction were identified in hepatocytes (AML12 cells) following the OA administration.