PI3K

Recent Findings on PI3K

• A pH-responsive, cRGD-modified liposomal system was developed to co-deliver the membrane-active immunogenic cytotoxic peptide FR and the PI3Kγ inhibitor IPI549. The system, designated FP2@PSLR, was designed to coordinate tumor-microenvironment remodeling with antitumor immunotherapy. This work combines PI3Kγ inhibition with a liposome-based delivery platform and an immunogenic cytotoxic agent, placing PI3K among target combinations intended to modify the tumor microenvironment rather than solely suppress tumor-cell proliferation 42605855Aug.

• In a cerebral ischemia–reperfusion injury study, a Danshensu derivative was investigated in relation to the PI3K-AKT-CREB signaling pathway. In vitro inhibition experiments in rat brain microvascular endothelial cells (RBMVECs) used the PI3K inhibitor LY294002 and the CREB inhibitor 666-15 to further test pathway involvement. The study therefore used pharmacological inhibition to examine whether PI3K and CREB participated in the protective mechanism associated with the Danshensu derivative 42069160May.

• Vitamin D was investigated as a regulator of lipid metabolism in granulosa cells in a model of polycystic ovary syndrome. The study evaluated FABP3-associated PI3K/Akt signaling together with lipid-metabolism regulators and cellular phenotypes, including FABP3, FASN, ATGL, PPARγ, phosphorylated PI3K, phosphorylated Akt, cell viability, proliferation, free fatty acid levels, and perilipin-2 expression. PI3K/Akt was thus examined as part of a signaling network connecting vitamin D, lipid handling, and granulosa-cell function 42302377Jun.

• A study of polysaccharides extracted from Notopterygium franchetii examined how extraction-driven structural differences influenced antidiabetic activity. In insulin-resistant HepG2 cells, the polysaccharide fraction ANP-1 increased glucose uptake and glycogen synthesis, accompanied by activation of IRS1/PI3K/AKT signaling. These findings place PI3K within a metabolic signaling axis associated with cellular insulin responsiveness and glucose storage 42493156Jul.

• In breast cancer models resistant to cyclin-dependent kinase 4/6 inhibitors, PI3K inhibition was investigated alongside strategies directed at casein kinase 1α-mediated FADD phosphorylation. The study reported that either inhibition of FADD phosphorylation with the CK1α degrader DEG-77 or PI3K inhibition restored sensitivity to CDK4/6 inhibitors in selected resistant cells. This work connects PI3K activity with therapeutic resistance and with the regulation of treatment response in cancer cells 42518285Jul.

• Sini Decoction was studied in mice subjected to forced-swimming stress as a treatment for anxiety-related phenotypes. Network pharmacology and experimental validation identified the PI3K/Akt signaling pathway as a core mechanism; the study reported that Sini Decoction reduced PI3K and Akt protein expression, while a PI3K agonist reversed this effect. The work also identified 6-gingerol and licochalcone B as compounds showing stable binding to core targets in the study’s molecular analyses 42044778Apr.

• In a rheumatoid arthritis study, Zhiwang decoction was evaluated for effects on inflammation and macrophage polarization. The proposed mechanism involved cellular communication network factor 1 (CCN1) and the PI3K/AKT phosphorylation pathway, with experimental analyses focused on CCN1 expression, macrophage M1 polarization, and pathway activity. PI3K/Akt was therefore examined as a mediator linking a therapeutic decoction to inflammatory responses and macrophage behavior 42081959May.

• Phytochemicals from Pistacia integerrima were investigated for anti-proliferative and anti-migratory activity in lung cancer through analyses involving PI3K, AKT1, and KRAS. Molecular docking evaluated interactions between major phytochemicals and oncogenic targets, reporting favorable calculated binding affinities for compounds including kaempferol, β-sitosterol, luteolin, and quercetin. The reported docking values included −9.4 kcal/mol for PI3K, −7.6 kcal/mol for AKT1, and −8.5 kcal/mol for KRAS; MMP9 was also included among the evaluated targets 42730982Sep.

• An asymmetric “spear-shield” hydrogel was developed to promote diabetic foot-ulcer healing by modulating macrophage autophagy. The study reported that artemisinin and Cu²⁺ activated macrophage autophagy through both the PI3K/AKT/mTOR and AMPK/mTOR pathways. PI3K was therefore investigated as part of a combined signaling framework connecting biomaterial-assisted wound healing, macrophage function, autophagy, and tissue repair 42409241Jul.