Pterostilbene as a pyroptosis inducer and tumor microenvironment regulator inhibits glioblastoma and enhances the efficacy of immunotherapy.

Glioblastoma (GBM) is a highly invasive tumor type associated with a high mortality rate, and the efficacy of traditional chemotherapy, targeted therapy, and immunotherapy for GBM remains limited. Therefore, there is an urgent need to develop novel therapeutic agents and strategies to combat GBM effectively. The upregulation of the pivotal pyroptosis protein GSDME in GBM suggests that harnessing cellular pyroptosis may be a promising approach for anti-GBM treatment.

Corrigendum: ANGPTL8 promotes adipogenic differentiation of mesenchymal stem cells: potential role in ectopic lipid deposition.

[This corrects the article DOI: 10.3389/fendo.2022.

Triphenylphosphine-Initiated Ring-Opening Polymerization for α-Helical Polypeptides and Application in Constructing Artificial Ion Channels.

In this study, we have screened out an effective triphenylphosphine-derived initiator () for efficient ring-opening polymerization of α-amino acid -carboxyanhydrides (NCA ROP) and demonstrated the potential of the prepared helical polypeptide as an efficient ion channel. By optimizing polymerization conditions, exhibited precise control over the molecular weight and polydispersity index for the prepared polypeptides, the universality for different NCA monomers, and the ability to form α-helical secondary structures. By further incorporating ion binding groups and regulating the molecular length, α-helical polypeptide was capable of inserting into lipid bilayers and possessing the function of ion transport (H/K antiport) via a channel mechanism (EC = 12.

BRG1 improves reprogramming efficiency by enhancing glycolytic metabolism.

BRG1 has been found to promote the generation of induced pluripotent stem cells (iPSCs) by regulating epigenetic modifications or binding to transcription factors, however, the role of BRG1 on the cellular metabolism during reprogramming has not been reported. In this study, we found that BRG1 improved the efficiency of porcine iPSC generation, and upregulated the expression of pluripotency-related factors. Further analysis revealed that BRG1 promoted cellular glycolysis, and increased levels of glycolysis-related metabolites.

Photoresponsive prodrug-based liposomes for controllable release of the anticancer drug chlorambucil.

The on-demand delivery and release of chemotherapeutic drugs have attracted great attention, among which photoresponsive prodrug systems have shown specific advantages for effective cancer treatment due to their spatiotemporal control, non-invasive nature and easy operation. Unlike the traditional strategy of physical encapsulation of drugs in liposomes, we herein report a biomimetic and photoresponsive drug delivery system (DDS) based on a lipid prodrug liposomal formulation (LNC), which combines the features of the prodrug and nanomedicines, and can realize photocontrollable release of anticancer drugs. The lipid prodrug comprises three functional moieties: a single-arm phospholipid (Lyso PC), an -nitrobenzyl alcohol (NB) and chlorambucil (CBL).

Trimethylamine N-oxide promotes the proliferation and migration of hepatocellular carcinoma cell through the MAPK pathway.

Trimethylamine-n-oxide (TMAO) is a metabolite of intestinal flora following the consumption of phosphatidylcholine-rich foods. Clinical cohort studies have shown that plasma TMAO may be a risk factor for cancer development, including hepatocellular carcinoma (HCC), but fundamental research data supporting this hypothesis are lacking. In this study, HCC cells were treated with TMAO in vivo and in vitro to evaluate the effect on some indicators related to the malignancy degree of HCC, and the relevant molecular mechanisms were explored.

ANGPTL8 deficiency attenuates lipopolysaccharide-induced liver injury by improving lipid metabolic dysregulation.

Liver injury is closely related to poor outcomes in sepsis patients. Current studies indicate that sepsis is accompanied by metabolic disorders, especially those related to lipid metabolism. It is highly important to explore the mechanism of abnormal liver lipid metabolism during sepsis.

ABI3BP promotes renal aging through Klotho-mediated ferroptosis.

The aging process of the kidneys is accompanied with several structural diseases. Abnormal fiber formation disrupts the balance of kidney structure and function, causing to end-stage renal disease and subsequent renal failure. Despite this, the precise mechanism underlying renal damage in aging remains elusive.

NSUN2 relies on ALYREF to regulate Nrf2-mediated oxidative stress and alleviate Dox-induced liver injury.

Background: Doxorubicin (Dox) is associated with various liver injuries, limiting its clinical utility. This study investigates whether NSUN2 participates in Dox-induced liver injury and the associated molecular mechanism.

Methods: In vivo and in vitro liver cell injury models were constructed based on Dox therapy.

Jinyinqingre Oral Liquid alleviates LPS-induced acute lung injury by inhibiting the NF-κB/NLRP3/GSDMD pathway.

Acute lung injury (ALI) is a prevalent and severe clinical condition characterized by inflammatory damage to the lung endothelial and epithelial barriers, resulting in high incidence and mortality rates. Currently, there is a lack of safe and effective drugs for the treatment of ALI. In a previous clinical study, we observed that Jinyinqingre oral liquid (JYQR), a Traditional Chinese Medicine formulation prepared by the Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, exhibited notable efficacy in treating inflammation-related hepatitis and cholecystitis in clinical settings.

Dual role of ANGPTL8 in promoting tumor cell proliferation and immune escape during hepatocarcinogenesis.

The interplay between hepatocellular carcinoma (HCC) cells and the tumor microenvironment is essential for hepatocarcinogenesis, but their contributions to HCC development are incompletely understood. We assessed the role of ANGPTL8, a protein secreted by HCC cells, in hepatocarcinogenesis and the mechanisms through which ANGPTL8 mediates crosstalk between HCC cells and tumor-associated macrophages. Immunohistochemical, Western blotting, RNA-Seq, and flow cytometry analyses of ANGPTL8 were performed.

Boosting Glioblastoma Therapy with Targeted Pyroptosis Induction.

Glioblastoma (GBM) is a highly aggressive cancer that currently lacks effective treatments. Pyroptosis has emerged as a promising therapeutic approach for cancer, but there is still a need for new pyroptosis boosters to target cancer cells. In this study, it is reported that Aloe-emodin (AE), a natural compound derived from plants, can inhibit GBM cells by inducing pyroptosis, making it a potential booster for pyroptosis-mediated GBM therapy.

CircRRAS2 promotes myogenic differentiation of bovine MuSCs and is a novel regulatory molecule of muscle development.

The proliferation and myogenic differentiation of muscle stem cells (MuSCs) are important factors affecting muscle development and beef quality. There is increasing evidence that circRNAs can regulate myogenesis. We found a novel circRNA, named circRRAS2 that is significantly upregulated in the differentiation phase of bovine MuSCs.

A rigid-axle-based molecular rotaxane channel facilitates K/Cl co-transport across a lipid membrane.

Inspired by the design criteria of heteroditopic receptors for ion-pair binding, we herein describe a new strategy to construct a rotaxane transporter (RR[2]) for K/Cl co-transport. The use of a rigid axle improves the transport activity with an EC value of 0.58 μM, presenting a significant step toward developing rotaxane artificial channels.

NSUN2 alleviates doxorubicin-induced myocardial injury through Nrf2-mediated antioxidant stress.

Doxorubicin (DOX) is a commonly used antitumor drug, but its application has been limited because of its strong cardiac damage. This study aims to explore the role of NSUN2 in DOX-induced heart injury. C57BL/6J mice were intraperitoneally injected with 20 mg/Kg DOX to induce heart injury.

TGF-β1 suppresses de novo cholesterol biosynthesis in granulosa-lutein cells by down-regulating DHCR24 expression via the GSK-3β/EZH2/H3K27me3 signaling pathway.

Cholesterol is a precursor to steroid hormones and can be obtained from serum LDL or de novo synthesis in steroidogenic cells. Before luteinizing hormone (LH) surge-induced ovulation, follicles remain avascular, and cholesterol required for progesterone production in granulosa cells (GCs) is derived from de novo biosynthesis. Previous studies have verified that the intrafollicular TGF-β1 plays inhibitory roles in GCs luteinization, vascularization, and progesterone production.

ANGPTL8 accelerates liver fibrosis mediated by HFD-induced inflammatory activity via LILRB2/ERK signaling pathways.

Introduction: High calorie intake is known to induce nonalcoholic fatty liver disease (NAFLD) by promoting chronic inflammation. However, the mechanisms are poorly understood.

Objectives: This study examined the roles of ANGPTL8 in the regulation of NAFLD-associated liver fibrosis progression induced by high fat diet (HFD)-mediated inflammation.

HIV-1 Tat Protein-Mediated Inflammatory Response Inhibits the Erythroid Hematopoietic Support Function of Bone Marrow Mesenchymal Stem Cells.

Although combination antiretroviral therapy is widely used to treat HIV-1 infection, anemia affects the health and quality of life in a large number of these patients. The proliferation and differentiation of bone marrow mesenchymal stem cells (BMSCs), as important support cells in the hematopoietic microenvironment, can be affected by HIV-1 Tat protein. In this study, we explored the mechanism underlying the effect of Tat protein on the hematopoietic support function of BMSCs in erythroid commitment.

ANGPTL8 is a negative regulator in pathological cardiac hypertrophy.

Pathological cardiac hypertrophy is an independent risk factor for heart failure and is considered a target for the treatment of heart failure. However, the mechanisms underlying pathological cardiac hypertrophy remain largely unknown. We aimed to investigate the role of angiopoietin-like protein 8 (ANGPTL8) in pathological cardiac hypertrophy.