KIM1 (Kidney injury molecule 1)

However, TRG therapy restored renal impairments via regulating antioxidative, anti-apoptotic, anti-inflammatory, and histo-architecture. Our findings were strongly supported by in-silico findings that demonstrated the potential binding of TRG with key regulatory genes.

This first direct comparison confirms rutin's superior efficacy over GA in mitigating CCl₄-induced nephrotoxicity via antioxidant and anti-inflammatory pathways. The integrated in silico and in vivo approach validates their mechanisms, highlighting rutin's prophylactic potential.

Mechanistically, NMN elevated kidney NAD+ levels and enhanced SIRT1 expression. These findings demonstrate that NMN protects against CIS-AKI by activating the NAD+-SIRT1 pathway, thereby reducing oxidative stress and inflammation, and suggest its potential as a therapeutic strategy for CIS-AKI.

Our works establish Homo-SELEX as a breakthrough strategy for homologous protein screening, with S7 serving as a robust, species-agnostic molecular probe for KIM-1 detection. This advancement holds significant promise for non-invasive diagnostics and targeted therapies for KIM-1-associated pathologies.

Such findings were supported by renal histological features improvement. In conclusion, CAR counteracted the renal damage induced by DOX via suppressing oxidative stress, inflammatory response, and apoptosis through downregulation of PI3K/Akt/mTOR and Bax/Bcl2 and upregulation of Nrf2/HO-1 signals.

The LT-025 displayed superior cytotoxicity to the metastatic RCC cells, then standard RCC treatment by sunitinib...The combination therapy also showed an increased tumor growth inhibition in preclinical mouse model studies. A carefully designed KIM-1 targeting ADC can emerge as an effective treatment method for metastatic RCC.

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.

Piribedil effectively protects against CP-induced nephrotoxicity by modulating AMPK/SIRT1 and related oxidative and inflammatory pathways, supporting its potential use in drug-induced kidney injury.

Among the evaluated biomarkers, KIM-1 demonstrated the strongest potential as an early biochemical indicator of renal allograft dysfunction. Its rapid post-transplant elevation underscores its sensitivity to early tubular injury. Further prospective validation in larger, multicenter cohorts is warranted.

These findings highlight that both AD-MSCs and their exosomes confer significant therapeutic effect against CTX-induced hepatorenal toxicity through modulation of apoptosis, inflammation, and oxidative stress pathways. Importantly, AD-MSCs-Exos demonstrated superior therapeutic efficacy compared to AD-MSCs in restoring antioxidant defenses and attenuating inflammatory and apoptotic responses in both liver and kidney tissues.

Overall, adjuvant pembrolizumab is practice-changing for high-risk clear-cell RCC, while neoadjuvant and perioperative approaches remain investigational. Advancing the field will require biomarker‑driven patient selection supported by adaptive or platform trial designs capable of rapidly evaluating multiple strategies.

In conclusion, our study is the first to demonstrate that despite the significant differences in the amount of smoke inhaled, both Occ-HS or Reg-HS inhalation deteriorate kidney function and induce oxidative damage, inflammatory response, DNA injury, and mitochondrial impairment with modulation of the MAPK signaling. These findings highlight the importance of further research into the public health risks associated with occasional hookah smoking.