P4, N=15, Completed, Children's Hospital of Fudan University | Recruiting --> Completed | N=10 --> 15

Further, treatments with drugs such as IFN-γ, 2-DG, and simvastatin modulate the density of PD-L1 without affecting its monomeric state...Finally, we observed that PD-L1 forms nanoclusters at cell-cell conjugation sites between breast cancer cells and T cells. Overall, these findings based on STORM extend our understanding of the nanoscale organization of PD-L1 on the membrane.

Rosuvastatin reduces inflammation by lowering TNF-α, IL-1β, IL-6, CRP while increasing neo-angiogenesis, fibroblast reactions and microenvironmental protection in burn wounds. These effects promote repair and positively impact burn wound healing.

P1, N=32, Active, not recruiting, Genentech Inc. | Recruiting --> Active, not recruiting

P3, N=103, Not yet recruiting, Daiichi Sankyo Europe, GmbH, a Daiichi Sankyo Company

P2, N=150, Active, not recruiting, OHSU Knight Cancer Institute | Recruiting --> Active, not recruiting

To address this limitation, we developed a lipid-prodrug nanoamplifier (SIM-SS-LA NAs), composed of disulfide-linked linoleic alcohol and simvastatin (SIM) to enhance ferroptosis...Notably, the released LA acts as an exogenous substrate, substantially increasing lipid peroxide accumulation and synergizing with SIM-mediated GPX4 inhibition to amplify ferroptosis. As expected, the lipid-prodrug nanoamplifier showed potent ferroptosis-driven antitumor activity in a 4T1 breast tumor-bearing mouse model, offering an efficient nanotherapeutic strategy for ferroptosis-based cancer therapy.

An AS model was established in apolipoprotein E knockout(ApoE~(-/-)) mice, which were divided into a normal group, an model group, low/medium/high-dose DZTMW groups, and an atorvastatin positive control group...Its mechanism may involve the regulation of hepatic lipid metabolism by its in vivo active components to ameliorate the "phlegm-turbidity" pathology and reduce liver injury, and the inhibition of systemic inflammation to alleviate the "blood stasis" process. The study can provide a modern biological basis for the theory of "phlegm-stasis intermingling".

The rats were randomly assigned to the following groups: model group, atorvastatin calcium group(4.8 mg·kg~(-1)), low-, medium-, and high-dose Tanyu Tongzhi Optimization Decoction(TYTZD) groups(3.6, 7.2, and 14.4 g·kg~(-1)), and a normal diet control group...Western blot indicated that TYTZD reduced TLR4, p-NF-κB, and IL-1β protein expression in liver tissue. In conclusion, TYTZD may exert anti-hyperlipidemic effects through regulation of core targets such as ITGAM, TLR4, and APOC2, and by modulating the TLR4/NF-κB signaling pathway to intervene in inflammatory responses and cholesterol metabolism, thereby achieving multi-target, multi-pathway therapeutic effects against hyperlipidemia.

Rats were divided into five groups(n=15 each), i.e., control, model, QBPF, QBPF + nigericin(NLRP3 activator), and simvastatin groups...In conclusion, QBPF attenuates lung function decline, suppresses inflammatory responses, alleviates pulmonary vascular remodeling, and intervenes in the disease progression of COPD complicated by PH in rats. Its mechanisms may be related to modulating the NLRP3/Caspase-1/GSDMD pathway to inhibit PAAF pyroptosis.

An atherosclerosis(AS) model was established in ApoE~(-/-) mice by feeding a high-fat diet for 14 weeks, and mice were randomly divided into a model group, MGFK high-dose group, MGFK low-dose group, and atorvastatin group...Furthermore, MGFK decreased the apoptosis rate within plaques, upregulated B-cell lymphoma-2(BCL-2) expression, downregulated BCL-2-associated X protein(BAX) and cleaved caspase-3, and promoted the phosphorylation of PI3K and AKT. These findings suggest that MGFK exerts anti-atherosclerotic effects potentially by regulating the PI3K/AKT signaling pathway, thereby reducing apoptosis within plaques, lowering levels of inflammatory cytokines and blood lipids, and attenuating plaque size, lipid content, and foam cell formation.