TIMP1 (Tissue inhibitor of metalloproteinases 1)

Male sex was associated with a higher risk of kidney failure and mortality, despite adjustment for demographic, clinical, and treatment factors. Males had higher levels of inflammatory and extracellular matrix deposition biomarkers. In contrast, females showed higher levels of matrix turnover and degradation markers. After adjustment for these biomarker differences, the elevated risk associated with male sex was eliminated, suggesting a biological basis for the observed sex difference in outcomes.

PF effectively attenuated hepatic metabolic dysregulation, inflammation, and fibrotic activation through inhibition of this pathway. Our work provided the first evidence establishing the SYK/SH3BP2 signaling axis as a pivotal pathway in MASLD progression, unveiling novel therapeutic targets while furnishing a mechanistic foundation for PF's potential application in MASLD treatment.

We constructed and validated a novel gene signature related to manganese metabolism in GBM patients. This gene signature not only reliably predicts the clinical outcomes of GBM patients but also has the potential to guide the provision of new treatment options for these patients.

This multi-level and bioinformatics study identifies TIMP1 as a cross-disease regulator with context-dependent functions. TIMP1 serves as a potential prognostic and diagnostic biomarker in digestive cancers, a therapeutic stratification marker for epigenetic interventions, and a candidate mediator linking tumor biology with cardiovascular disorders such as atherosclerosis and heart failure.

TIMP1 was further identified as a critical oncogene in patients with colorectal cancer. Our results provide a theoretical basis for subsequent exosome-based preclinical trials.

The combination exhibits a clear synergistic effect and demonstrates strong potential as a supportive therapeutic strategy. These findings warrant further in vivo and clinical-level investigations to evaluate the translational applicability of sitagliptin in cervical cancer therapy.

In contrast to LEV, VPA did not correct these molecular alterations induced by orthodontic force and, in several parameters, further exacerbated them. In conclusion, molecular data from the animal model indicate that LEV plays a protective role against orthodontic force by reducing excess levels of oxidative stress, apoptosis, and inflammation and homeostatic pathways.

Collectively, these findings demonstrate that E. cava-derived phlorotannins exert anti-metastatic effects through dual regulation of IL-17RA/Act1 and ERK1/2 signaling pathways, offering mechanistic insight into their therapeutic potential against inflammation-driven malignancies.

Irinotecan (CPT-11), a topoisomerase I inhibitor converted to its active metabolite SN-38, has emerged as a potential chemotherapeutic alternative for GBM due to its distinct mechanism of action and non-cross-resistance with temozolomide (TMZ). Collectively, these developments mark a translational shift from empirical cytotoxic therapy toward a modular, precision-engineered platform. The integration of biomarker discovery, molecularly rational combinations, and locoregional delivery systems positions irinotecan as a key component of next-generation GBM treatment paradigms, with the potential to overcome historical barriers such as BBB impermeability and therapeutic resistance.

Circulating EVs are a promising biomarker source in CRLM. However, with only limited studies to date, further research is needed to substantiate these findings.

QHYD ameliorates alcoholic hepatic fibrosis through multi-targeted mechanisms: inhibiting MAPK/TLR4-MyD88 inflammatory pathways, restoring hepatic metabolism via l-histidine, and modulating gut microbiota. Its favorable safety profile and efficacy across diverse models support QHYD as a promising therapeutic candidate, with l-histidine serving as a key mediating metabolite.

In pre-clinical PC, TIMP-1/CISS proves targetable through combined inhibition of upstream kinases with clinically approved drugs trametinib and nintedanib. Collectively, CISS represents a ubiquitous signature of pro-tumor immunoinstruction with actionable diagnostic and therapeutic potential across human cancers.