HMOX1 expression

Oxaliplatin combined with KLF5 inhibitor significantly potentiated cell death in vitro and inhibited tumor growth in vivo compared with either treatment alone. These results reveal a critical role of KLF5 in sensitized chemotherapy of pancreatic cancer, and suggest that ferroptosis combined with platinum-based chemotherapy rather than gemcitabine-based chemotherapy is expected to bring better therapeutic effects.

P=N/A, N=200, Recruiting, First Affiliated Hospital of Army Medical University; First Affiliated Hospital of Army Medical University

Expression of the HMOX1 gene was markedly increased under CMSP treatment, while lower expression was observed in cancer tissue compared to adjacent tissue. CMSP triggers mitochondrial dysfunction via HMOX1 activation, leading to ferroptosis in SCLC cells, underscoring its potential as a therapeutic agent for SCLC.

Finally, Mapk8, as a ferroptosis driver, was remarkably elevated in E. faecalis-infected Gsta4-deficient macrophages. These results suggest that Gsta4 inactivation blocks MIBE by eliminating macrophages, thereby attenuates E. faecalis-induced colitis and CRC.

In conclusion, our study provides insight into the pathogenic mechanisms of osteocyte death induced by melanoma bone metastasis, with a specific focus on ferroptosis and its regulation. This would enhance our comprehension of melanoma-induced osteocyte death.

In addition, epicatechin increased the expression of nuclear factor erythroid-2 related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1). We therefore conclude that epicatechin protected EMB-induced liver injury by preventing ferroptosis through activating Nrf2.

ME promoted ferroptosis in HCT116 and LOVO cells, reversing ROS, lipid peroxidation and GSSG/GSH radio level. In general, the findings stated that the polysaccharides provided effects of inducing colon cancer ferroptosis, uncovering potential function of ME from maggot as a candidate compound.

These results suggest a novel mechanism for brain reelin depletion in schizophrenia. Containment of the astrocytic HO-1 cascade by pharmacological or other means may protect against stress-induced brain reelin depletion in schizophrenia and other neurodevelopmental disorders.

Expression of nuclear HMOX1 was increased in both cell lines, with the CuPhTh2 complex being the most active. Inhibition of HMOX1 activity significantly decreased the IC50 values of these copper complexes suggesting that HMOX1 inhibition may alter treatment outcomes in PDAC.

Expression of nuclear HMOX1 was increased in both cell lines, with the CuPhTh2 complex being the most active. Inhibition of HMOX1 activity significantly decreased the IC50 values of these copper complexes suggesting that HMOX1 inhibition may alter treatment outcomes in PDAC.

Stretch induced significantly Hmox1 transcriptional activity under NG conditions and Socs3 under HG conditions especially in tenocytes of DMT2 rats. The response of tenocytes to TNFα and cyclic stretch depends on glucose supply and origin suggesting their irreversible impairment by DMT2.

By modulating key pathways and endocannabinoid system components, TUR demonstrates potential as a novel therapeutic agent for OA management. Future studies could explore its clinical applications and further validate its molecular mechanisms in vivo.