A lactate-HIF1α-VDR positive feedback loop drives protective SPP1⁺ macrophage differentiation to inhibit schistosomiasis-induced liver fibrosis

NUPR1-positive tumor-associated macrophages facilitate the progression of hepatocellular carcinoma via ferroptosis resistance.

BACKGROUND Tumor-associated macrophages (TAMs) are major contributors to the immunosuppressive microenvironment of hepatocellular carcinoma (HCC). Nuclear protein 1 (NUPR1) is a stress-responsive regulator implicated in tumor progression; however, whether it functionally controls ferroptosis-associated stress adaptatio...

Role of HIF1α in FXR-mediated protection and anti-inflammatory macrophage polarization in parenteral nutrition-associated cholestasis.

Parenteral nutrition-associated cholestasis (PNAC) arises from suppressed FXR signaling and macrophage activation driven by intestinal LPS and PN-derived phytosterols. We investigated whether tissue hypoxia and HIF1α signaling play a role in FXR-mediated protection in PNAC. PNAC mouse intrahepatic mononuclear cells (IH...

HIF-1α-ASS1 axis drives reprogramming of arginine metabolism controls hepatic stellate cell activation in hepatic fibrosis.

ABRL8301 acts as a pharmacologic inducer of ASS1 and arginine biosynthesis, inhibiting EMT and fibrotic progression while enhancing anticancer therapy and support ABRL8301 as a promising antifibrotic and tumor-sensitizing agent in hepatic fibrosis.

Hypoxia confers ferroptosis resistance in glioma cells via HIF-1α/SREBP1-mediated regulation of lipid metabolism

The role of the HIF-1α-SREBP1-FASN/SCD1 signaling axis in ferroptosis regulation in glioma is systematically elucidated, providing important theoretical foundations and experimental support for developing HIF-1α-targeted ferroptosis therapies.

FATP5 loss in hepatocellular carcinoma cells orchestrates tumor-promoting microenvironment by inducing passive long-chain fatty acid accumulation within tumor-associated endothelial cells.

HIFU-driven remodeling of fi brotic perivascular myeloid niches in hepatocellular carcinoma: implications for PD-1/PD-L1 blockade