Acinar Cell-Derived Extracellular Vesicle MiRNA-183-5p Aggravates Acute Pancreatitis by Promoting M1 Macrophage Polarization Through Downregulation of FoxO1.

Acute pancreatitis (AP) is a common cause of a clinically acute abdomen. Crosstalk between acinar cells and leukocytes (especially macrophages) plays an important role in the development of AP. However, the mechanism mediating the interaction between acinar cells and macrophages is still unclear.

Comprehensive Analysis of Necroptosis in Pancreatic Cancer for Appealing its Implications in Prognosis, Immunotherapy, and Chemotherapy Responses.

Necroptosis represents a new target for cancer immunotherapy and is considered a form of cell death that overcomes apoptosis resistance and enhances tumor immunogenicity. Herein, we aimed to determine necroptosis subtypes and investigate the roles of necroptosis in pancreatic cancer therapy. Based on the expression of prognostic necroptosis genes in pancreatic cancer samples from TCGA and ICGC cohorts, a consensus clustering approach was implemented for robustly identifying necroptosis subtypes.

ATG7-enhanced impaired autophagy exacerbates acute pancreatitis by promoting regulated necrosis via the miR-30b-5p/CAMKII pathway.

The present study was performed to explore whether and how impaired autophagy could modulate calcium/calmodulin-dependent protein kinase II (CAMKII)-regulated necrosis in the pathogenesis of acute pancreatitis (AP). Wistar rats and AR42J cells were used for AP modeling. When indicated, genetic regulation of CAMKII or ATG7 was performed prior to AP induction.

lncRNA FGD5‑AS1 promotes breast cancer progression by regulating the hsa‑miR‑195‑5p/NUAK2 axis.

Breast cancer is the second most prevalent cancer in women worldwide. Long non‑coding RNAs (lncRNAs) have been identified as important regulators of tumorigenesis and tumor metastasis. lncRNA FGD5‑AS1 has been previously reported as a carcinogenic gene, however its role in breast cancer has yet to be investigated.

[Molecular mechanism of effect of wenban humai granule on stability of atheromatous plaque].

Objective: To explore the molecular mechanism of wenban humai granule (WHG) in stabilizing atheromatous plaque, by observing its effect on the collagen degradation and synthesis imbalance manner in the fibrous cap of the plaque.

Methods: Atherosclerosis (AS) rabbit model established by feeding high fat diet. The changes of protein and mRNA expression of macrophage CD68, metalloproteinase-1 (MMP-1), alpha-smooth muscle actin (alpha-SMA) and collagen I (C-I) in model rabbits' neo-genesic intima were determined by immunohistochemical stain and in situ hybridization methods before and after treatment as well as before and after modeling.