MAPK8 (Mitogen-activated protein kinase 8)

Our study demonstrates that EG and SIL treatments effectively alleviate 5-FU-induced acute liver injury by modulating 5-FU catabolism and suppressing the mitogen-activated protein kinase and NF-κB signaling pathways in rats.

Study heterogeneity, variable antibody scoring, and limited assessment of senescence-associated beta-galactosidase and secretory mediators restricted cross-study comparability. Standardized, spatially resolved profiling may refine risk stratification and support senescence-targeted prevention and therapy in keratinocyte cancers.

Subsequent SHAP analysis revealed SRC, HSP90AB1, HSP90AA1 and CDK1 as the key contributors to prognostic prediction, with each being highly expressed in BC and linked to poor clinical prognosis. Notably, among all chemicals screened, Disperse Yellow 3 exhibited the strongest binding affinity to these four key targets, demonstrating the strongest association with BC risk.

LCM treatment effectively mitigated these deleterious effects through multi-target protective mechanisms including c-jun N-terminal kinase 1(JNK1)-mediated apoptosis inhibition, HO-1 upregulation, IL-6/ signal transducer and activator of transcription 3 (STAT-3) signaling suppression, prevention of p-JNK1/STAT-3 crosstalk, and AR preservation. This study establishes LCM's multi-target protective efficacy, supporting its potential as a safer antiepileptic alternative providing dual benefits of seizure control and reproductive preservation during chemotherapy.

Our findings highlight the beneficial role of TGP in preserving synaptic structural integrity and functionality and suggest a novel mechanism of synaptic dysfunction implicated in the pathophysiology of PSD. The results indicate that the regulation of the ERS signaling pathway by TGP presents therapeutic promise for the treatment of PSD.

Our findings suggest that UPM exposure alone elicited limited stress-adaptive antioxidant responses without effective cytoprotection. In contrast, araliadiol treatment independently activated robust antioxidant and cytoprotective signaling. Moreover, under UPM exposure, araliadiol further enhanced cellular defense through the activation of the Nrf2 and JNK-AP-1 signaling pathways. These results highlight the therapeutic potential of araliadiol as a dermoprotective agent derived from Centella asiatica, particularly in mitigating pollutant-induced skin damage.

The mechanisms involve suppressing ROS generation, maintaining mitochondrial membrane stability, enhancing cell viability, migration, and proliferation, as well as inhibiting Jnk and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways. The findings highlight potential molecular targets and novel strategies for the clinical prevention and treatment of ATO-related toxicity .

In preclinical models of MASLD, treatment with AIK3a305 attenuated disease progression in animals fed either a HFD or a CDAA diet, as evidenced by improved liver histopathology, including reduced steatosis and inflammation. These findings position AIK3a305 as a promising therapeutic candidate for MASLD treatment.

In type 1 diabetes, autoimmune-mediated β-cell destruction is driven by inflammatory cytokines and dysregulated immune responses, while in type 2 diabetes, systemic and adipose tissue inflammation perpetuate insulin resistance and β-cell stress. Key molecular players, including toll-like receptors, the NLRP3 inflammasome, and the c-Jun N-terminal kinase (JNK) pathway, act as mediators between metabolic stress and inflammatory responses, emphasizing the bidirectional relationship between inflammation and hyperglycemia.

The bioactive compounds of nopal engage multiple biological pathways relevant to T2D and CRC, suggesting that this plant may serve as a promising pharmacological candidate for the management of these diseases.

These alterations were accompanied by reduced phosphorylation of heavy chain subunits of neurofilaments (NFs), major cytoskeletal elements linking myelin to the regulation of axonal caliber. Collectively, our findings reveal previously unrecognized effects of JNK3 deletion on OPC proliferation, NF phosphorylation, callosal axon caliber, and myelin thickness in vivo, suggesting a potential involvement of this kinase on myelinogenesis and/or myelin maintenance.

GCs protect against HIRI by activating the EPAC2-Rap1-Hippo-YAP-JNK axis to promote autophagy and suppress apoptosis. These findings provide mechanistic insight into the hepatoprotective actions of GCs and support their evidence-based ethnopharmacological use as a promising therapeutic approach for ischemic liver injury.