A layered structural Ni-MOF nanosheet has been obtained, exhibiting capacitances of 1518.8 F g−1 at 1 A g−1 and 244 mF cm−2 at 0.5 mA cm−2 as electrodes for supercapacitor and flexible all-solid-state asymmetric supercapacitor, respectively.
most frequent among females (the ratio between affected men and women is 2:1). [1,2] Approximately 270 000 new cases of RCC and 116 000 RCC-related deaths are reported worldwide per year. [3] Among the reported patients, clear cell RCC (ccRCC) cases account for 70-80%. [4] The cure rate of advanced ccRCC patients with a 5-year survival rate is as low as 11.7%, so efficient treatment is necessary. [5,6] Surgery is the most common treatment for ccRCC. However, with the high invasiveness and high resistance to chemotherapeutic agents, advanced ccRCC is difficult to cure once metastasis occurs. [7] In recent years, therapeutics focused on killing cancer cells via nanomaterial-based phototoxicities, such as photodynamic therapy (PDT) and photothermal therapy (PTT), have been widely studied. [8,9] PDT is an effective clinical approach that uses a photoactivatable compound as a photosensitizer and irradiation with appropriate wavelength light. Under illumination, the photosensitizer can be activated as a generator of reactive oxygen species (ROS) to kill cancer cells efficiently. PTT is also an effective means of cancer treatment, in which photothermal agents can catalyze the production of local heat under illumination to kill cancer cells. [9] PTT can increase the blood flow and Clear cell renal cell carcinoma (ccRCC) is a serious and tenacious disease. Photodynamic therapy (PDT) and photothermal therapy (PTT) are effective means of cancer treatment. However, PDT combined with PTT has been rarely reported in ccRCC treatment. In the present study, by developing the core-shell structured TiO 2 @red phosphorus nanorods (TiO 2 @RP NRs) as a photosensitizer, the feasibility and effectiveness of synchronous PDT and PTT treatments for ccRCC are demonstrated. The core-shell structured TiO 2 @ RP NRs are synthesized to drive the PDT and PTT for ccRCC, in which the RP shell is the sensitizer even in the near-infrared (NIR) region. The optimized TiO 2 @RP NRs can respond to NIR and produce local heat under irradiation. The NRs are estimated in ccRCC treatments via cell counting kit-8 assay, propidium iodide staining, qRT-PCR, and reactive oxygen species (ROS) probes in vitro, while terminal deoxynucleotidyl transferase dUTP nick-end labeling is conducted in vivo. After NIR irradiation, TiO 2 @RP NRs can efficiently kill ccRCC cells by producing local heat and ROS and cause low injury to normal kidney cells. Furthermore, treatment with TiO 2 @RP NRs and NIR can kill significant numbers of deep-tissue ccRCC cells in vivo. This work highlights a promising photo-driven therapy for kidney cancer.
Renal tubular epithelial cell (RTEC) death and renal interstitial inflammation are the most crucial pathophysiological changes in acute kidney ischemia/reperfusion injury (IRI). The microRNA (miR)-181d family plays diverse roles in cell proliferation, apoptosis and inflammation, but its renal target and potential role in IRI are unknown. Here, we showed that the expression of miR-181d-5p decreased and Krueppel-like factor 6 (KLF6) increased in a renal cell (HK-2) model of hypoxia/reoxygenation (H/R) injury and a mouse model of renal IRI. They were mainly distributed in the renal tubules. After renal IRI, miR-181d-5p overexpression significantly inhibited inflammatory mediators, reduced apoptosis and further improved renal function. KLF6 exacerbated RTEC damage and acted as a NF-κB co-activator to aggravate the renal IRI inflammatory response. Mechanistically, KLF6 was predicted as a new potential target gene of miR-181d-5p through bioinformatic analysis and luciferase reporter assay verification. After overexpressing miR-181d-5p and inhibiting KLF6, the role of miR-181d-5p was weakened on the renal damage improvement. In conclusion, miR-181d-5p upregulation produced protective antiapoptotic and anti-inflammatory effects against IRI in kidneys in vivo and H/R injury in HK-2 cells in vitro, and these effects were achieved by targeted inhibition of KLF6. Thus, our results provide novel insights into the molecular mechanisms associated with IRI and a potential novel therapeutic target.
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