Differential life cycle toxic effects and molecular mechanisms of Di(2-ethylhexyl) phthalate (DEHP) exposure on the female reproductive system.

Di(2-ethylhexyl) phthalate (DEHP), the most prevalent plasticizer worldwide, can enter the human body via various exposure pathways, including ingestion, inhalation, skin contact, and medical applications. It has been observed to exhibit characteristic patterns of accumulation in the female reproductive system. Research has demonstrated that DEHP poses a threat to reproductive health in females across various life stages.

Integrated Modeling of Composition-Resolved Source Apportionment and Dynamic Projection for Ozone Pollution in Datong.

Growing ozone (O) pollution in industrial cities urgently requires in-depth mechanistic research. This study utilized multi-year observational data from Datong City, China, from 2020 to 2024, integrating time trend diagnostics, correlation dynamics analysis, Environmental Protection Agency Positive Matrix Factorization 5.0 (EPA PMF 5.

Resveratrol: Great potential for alleviating di-2-ethylhexyl phthalate (DEHP)-induced testicular ferroptosis via the SIRT1-HIF-1α axis.

Background/objectives: Di-2-ethylhexyl phthalate (DEHP) is a universally used plasticizer and EDCs. Our previous studies verified that prolonged contact with DEHP induced detrimental impacts on reproductive physiology. Resveratrol (RES), a polyphenolic compound predominantly concentrated in Vitis vinifera epidermis, exhibits multifaceted pharmacological properties.

Shikonin treats Aspergillus fumigatus keratitis by activating autophagy and reducing fungal load.

The objective of this study was to explore the therapeutic potential of Shikonin (SK) in the treatment of fungal keratitis. Various tests conducted in this study were fluorescein sodium staining, Cell Counting Kit-8 (CCK-8), RT-PCR, Western blot (WB), immunofluorescence, and enzyme-linked immunosorbent assay (ELISA) methods. And the autophagic and phagocytic functions of RAW 264.

Reprogramming tumor-associated macrophages and blocking PD-L1 via engineered outer membrane vesicles to enhance T cell infiltration and cytotoxic functions.

The immunosuppressive tumor microenvironment (TME) critically undermines the efficacy of T cell-based tumor immunotherapy by impeding CD8 T cell infiltration and cytotoxic function, primarily through tumor-associated macrophages (TAMs) and immune checkpoint molecules such as programmed death ligand 1 (PD-L1). Here, we present a multifunctional nanoplatform, IN@OMV-PDL1nb, designed to simultaneously inhibit TAM-derived immunosuppressive metabolite itaconic acid (ITA) by targeting immune-responsive gene 1 (IRG1) and block PD-L1 within the TME. Engineered outer membrane vesicles (OMVs) serve as precision delivery vehicles for the IRG1 inhibitor IRG1-IN-1 (IN) and as carriers for PD-L1 nanobody release, activated by matrix metalloproteinase-2 (MMP-2).

The mitochondrial dysfunction regulated by JAK2/STAT3 pathway leads to the necroptosis in the renal cells under patulin exposure.

Patulin (PAT) is a common mycotoxin widely found in various agricultural products and fruits, which has obvious toxic effects on animals and humans. Some studies have shown that PAT can cause nephrotoxicity, but the exact mechanism remains to be elucidated. In the present study, we investigated PAT-induced nephrotoxicity and the possible molecular mechanisms involved in its action.

Palliative care with negative pressure wound therapy application in malignant wounds: a systematic review.

Objective: To synthesise and appraise the evidence for and benefits of palliative application of negative pressure wound therapy (NPWT) in malignant wounds.

Method: We performed a systematic review according to Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA). MEDLINE, Embase, Cochrane Library and trial registers (www.

Perfluorooctane sulfonate induced ferritinophagy via detyrosinated alpha tubulin-TRIM21-HERC2-regulated NCOA4 degradation in hepatocytes.

The persistent organic pollutant perfluorooctane sulfonate (PFOS) is demonstrated to induce hepatotoxicity through disrupting iron homeostasis and subsequent ferroptosis in hepatocytes. However, it is still elusive in the mechanisms underneath the dysfunctional iron metabolism caused by PFOS. In this study, we observed that PFOS activated the nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy in mice liver and human hepatocytes.

PFOS causes lysosomes-regulated mitochondrial fission through TRPML1-VDAC1 and oligomerization of MCU/ATP5J2.

Perfluorooctane sulfonate (PFOS), a listed persistent organic pollutant, poses risks to human health and is closely linked to chronic metabolic diseases. Although the role of mitochondrial fission in these diseases has garnered attention, whether and how PFOS induces mitochondrial fission remains obscure. Here, we found that PFOS induced mitochondrial fission, as demonstrated by the fragmentation of mitochondria and the upregulation of dynamin-related protein 1 (DRP1), phospho-DRP1 and mitochondrial fission protein 1 (FIS1) in human hepatocytes MIHA and mice liver.

CISD2-mediated mitochondrial dysfunction and iron redistribution contributes to ferroptosis in arsenic-induced nonalcoholic steatohepatitis.

Arsenic in the environment, such as sodium arsenic (NaAsO), is a frequently occurring hazard that has been linked to nonalcoholic steatohepatitis (NASH). Our prior research established the involvement of ferroptosis in arsenic-induced NASH, but the precise underlying mechanisms remain elusive. Here, we found that exposure to NaAsO had a suppressive effect on the expression of CDGSH iron-sulfur domain-containing protein 2 (CISD2) at the protein and gene levels, and overexpression of CISD2 inhibited NaAsO-induced ferroptosis and NASH.

Sodium arsenite induces islets β-cells apoptosis and dysfunction via SET-Rac1-mediated cytoskeleton disturbance.

Sodium arsenite (NaAsO), the most common form of inorganic arsenic prevalent in the environment, has been closely linked to islet β-cell dysfunction, a critical pathological hallmark of type 2 diabetes (T2D). Even though apoptosis plays a pivotal role in arsenic-induced islet β-cell dysfunction, the explicit underlying mechanisms remain elusive. Here, we have identified that the SET-Rac1 signaling pathway is instrumental in the apoptosis and dysfunction of islet β-cells induced by NaAsO.

PLIN5 contributes to lipophagy of hepatic stellate cells induced by inorganic arsenic.

Arsenic exposure triggers the activation of hepatic stellate cells (HSCs), resulting in liver fibrosis (LF). A significant decrease in lipid droplets marks the activation of HSCs. However, the exact underlying molecular mechanism remains elusive.

Arsenic inducible islet β-cell dysfunction and ferroptosis through mA-YTHDF2-dependent CHAC1 enhancement.

Arsenic, recognized as an environmental and food contaminant, has been linked to the dysfunction of islet β-cells, the primary lesions in type 2 diabetes (T2D). Ferroptosis, a regulated cell death pathway dependent on GPX4, has been implicated in arsenic-induced β-cell dysfunction. However, the underlying molecular mechanisms remain unclear.

ACSL4-mediated ZIP7-VDAC3 interaction regulates endoplasmic reticulum-mitochondria iron transfer in hepatocytes under PFOS exposure.

Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant with adverse health consequences. Our previous studies showed that PFOS caused an increase in mitochondrial iron and accelerated the expression of acyl-CoA synthetase long-chain family member 4 (ACSL4), one classic executor in the ferroptosis pathway. As ACSL4 is located in the mitochondria-associated endoplasmic reticulum (ER) membranes, here, we intended to further explore the role of ACSL4 in the inter-organelle iron crosstalk between ER and mitochondria under PFOS exposure.

The phosphorylation of Smad3 by CaMKIIγ leads to the hepatocyte pyroptosis under perfluorooctane sulfonate exposure.

Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant and accumulated in the liver of mammals. PFOS exposure is closely associated with the development of pyroptosis. Nevertheless, the underlying mechanism is unclear.

Lysosomal iron accumulation and subsequent lysosomes-mitochondria iron transmission mediate PFOS-induced hepatocyte ferroptosis.

Perfluorooctane sulfonate (PFOS) is known as a persistent organic pollutant. A significant correlation between PFOS and liver ferroptosis has been unveiled, but the precise mechanism needs to be elucidated. In prior research, we found that PFOS treatment provoked mitochondrial iron overload.

The role and mechanism of VDAC1 in type 2 diabetes: An underestimated target of environmental pollutants.

Type 2 diabetes (T2D) is a chronic metabolic disease that accounts for more than 90% of diabetic patients. Its main feature is hyperglycemia due to insulin resistance or insulin deficiency. With changes in diet and lifestyle habits, the incidence of T2D in adolescents has burst in recent decades.

The VDAC1 oligomerization regulated by ATP5B leads to the NLRP3 inflammasome activation in the liver cells under PFOS exposure.

As a persistent organic pollutant, perfluorooctane sulfonate (PFOS) has a serious detrimental impact on human health. It has been suggested that PFOS is associated with liver inflammation. However, the underlying mechanisms are still unclear.

Curcumin inhibits PAT-induced renal ferroptosis via the p62/Keap1/Nrf2 signalling pathway.

Patulin (PAT), the most common mycotoxin, is widespread in foods and beverages which poses a serious food safety issue to human health. Our previous research confirmed that exposure to PAT can lead to acute kidney injury (AKI). Curcumin is the most abundant active ingredient in turmeric rhizome with various biological activities.

Perfluorooctane sulfonate induces ferroptosis-dependent non-alcoholic steatohepatitis via autophagy-MCU-caused mitochondrial calcium overload and MCU-ACSL4 interaction.

The incidence of nonalcoholic steatohepatitis (NASH) is related with perfluorooctane sulfonate (PFOS), yet the mechanism remains ill-defined. Mounting evidence suggests that ferroptosis plays a crucial role in the initiation of NASH. In this study, we used mice and human hepatocytes L-02 to investigate the role of ferroptosis in PFOS-induced NASH and the effect and molecular mechanism of PFOS on liver ferroptosis.

Targeting STAT3 potentiates CDK4/6 inhibitors therapy in head and neck squamous cell carcinoma.

Anti-CDK4/6 therapy has been employed for the treatment for head and neck squamous cell carcinoma (HNSCC) with CDK4/6 hyperactivation, but the response rate is relatively low. In this study, we first showed that CDK4 and CDK6 was over-expressed and conferred poor prognosis in HNSCC. Moreover, in RB-positive HNSCC, STAT3 signaling was activated induced by CDK4/6 inhibition and STAT3 promotes RB deficiency by upregulation of MYC.

Sodium arsenite induces hepatic stellate cells activation by mA modification of TGF-β1 during liver fibrosis.

The compound known as Sodium arsenite (NaAsO), which is a prevalent type of inorganic arsenic found in the environment, has been strongly associated with liver fibrosis (LF), a key characteristic of nonalcoholic fatty liver disease (NAFLD), which has been demonstrated in our previous study. Our previous research has shown that exposure to NaAsO triggers the activation of hepatic stellate cells (HSCs), a crucial event in the development of LF. However, the molecular mechanism is still unknown.

Autophagy-dependent lysosomal calcium overload and the ATP5B-regulated lysosomes-mitochondria calcium transmission induce liver insulin resistance under perfluorooctane sulfonate exposure.

Perfluorooctane sulfonate (PFOS), an officially listed persistent organic pollutant, is a widely distributed perfluoroalkyl substance. Epidemiological studies have shown that PFOS is intimately linked to the occurrence of insulin resistance (IR). However, the detailed mechanism remains obscure.