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Cyclin J-CDK Complexes Limit Innate Immune Responses by Reducing Proinflammatory Changes in Macrophage Metabolism

[Science Signaling] Scientists demonstrated that cyclin J, a TLR-inducible member of the cyclin family, reduced cytokine production in macrophages by coordinately controlling glycolysis and mitochondrial functions.

Endothelial Plasticity Drives Aberrant Vascularization and Impedes Cardiac Repair after Myocardial Infarction

[Nature Cardiovascular Research] Investigators characterized vascular aberrancies induced by myocardial infarction (MI) and proposed to target acquired endothelial cell changes to normalize vessels and promote cardiac repair after MI.

Notch1 Activation of Jagged1 Contributes to Differentiation of Mesenchymal Stem Cells into Endothelial Cells under Cigarette Smoke Extract Exposure

[BMC Pulmonary Medicine] In vitro, Jagged1 was found to be activated by Notch1 in MSCs, resulting in the RBP-Jκ-dependent expression of Jagged1 mRNA, a response that was blocked by Notch1 inhibition.

HIF-1α Inhibitor PX-478 Preserves Pancreatic β Cell Function in Diabetes

[Science Translational Medicine] In response to PX-478 treatment, human islet organoids chronically exposed to high glucose presented improved stimulation index of glucose-induced insulin secretion.

A Novel HIF-2α Targeted Inhibitor Suppresses Hypoxia-Induced Breast Cancer Stemness via SOD2-mtROS-PDI/GPR78-UPRER Axis

[Cell Death & Differentiation] The authors illustrated that HIF-2α, but not HIF-1α, induced stemness in breast cancer cells under hypoxia through SOD2-mtROS-PDI/GRP78-UPRER pathway, linking mitochondrial metabolic state to endoplasmic reticulum response via mitochondrial reactive oxygen species level.

Doxorubicin Induced Immune Abnormalities and Inflammatory Responses via HMGB1, HIF1-α and VEGF Pathway in Progressive of Cardiovascular Damage

[Annals of Medicine] The authors comprehensively review the role of high-mobility group box 1 (HMGB1), hypoxia-inducible factor-1α (HIF-1α), and VEGF in doxorubicin-induced cardiovascular disease and its molecular mechanisms.