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Cellular senescence contributes to inflammatory kidney disease via the secretion of inflammatory and profibrotic factors. Protease‐activating receptor 2 (PAR2) is a key regulator of inflammation in kidney diseases. However, the relationship between PAR2 and cellular senescence in kidney disease has not yet been described. In this study, we found that PAR2‐mediated metabolic changes in renal tubular epithelial cells induced cellular senescence and increased inflammatory responses. Using an aging and renal injury model, PAR2 expression was shown to be associated with cellular senescence. Under in vitro conditions in NRK52E cells, PAR2 activation induces tubular epithelial cell senescence and senescent cells showed defective fatty acid oxidation (FAO). Cpt1α inhibition showed similar senescent phenotype in the cells, implicating the important role of defective FAO in senescence. Finally, we subjected mice lacking PAR2 to aging and renal injury. PAR2‐deficient kidneys are protected from adenine‐ and cisplatin‐induced renal fibrosis and injury, respectively, by reducing senescence and inflammation. Moreover, kidneys lacking PAR2 exhibited reduced numbers of senescent cells and inflammation during aging. These findings offer fresh insights into the mechanisms underlying renal senescence and indicate that targeting PAR2 or FAO may be a promising therapeutic approach for managing kidney injury. [ABSTRACT FROM AUTHOR]

Organic photodetectors (OPDs) based on non‐fullerene acceptors (NFAs) have received considerable attention because of their potential for use in various commercial applications as near‐infrared (NIR) light sensing platforms. However, recent OPDs suffer from low NIR photoresponse and large dark/noise currents with narrow bandgap organic photoactive materials. Herein, a π‐bridge molecular engineering strategy replacing alkoxythienyl with benzothiadiazole for ultra‐narrow bandgap (ultra‐NBG) NFAs is designed to achieve simultaneously high photoresponse at NIR region and low noise current density, thereby leading to excellent NIR (≈1050 nm) detectivity (D*). The newly synthesized ultra‐NBG NFAs, namely COB and CBT with optical bandgaps below 1.14 eV, present high responsivity (R) with 0.369 and 0.080 A W−1, respectively, at a wavelength of 1050 nm. Especially, with effectively suppressed noise current density, COB‐based OPD exhibits a high NIR (≈1050 nm) D* value of 2.18 × 1011 cm Hz1/2 W−1 at −0.5 V bias. The obtained R and D* values for these NFAs exceed or are comparable to those of a commercial Si photodetector at 1050 nm. This work provides important insight into the π‐bridge molecular engineering strategy for ultra‐NBG NFAs, which facilitate achieving highly sensitive NIR OPDs with high NIR photoresponse and low dark/noise current. [ABSTRACT FROM AUTHOR]

TiO2 polymorphs have distinct properties that are widely employed in various applications. However, mechanisms of transformations between these polymorphs are not fully understood, especially at atomic scale, inhibiting advancing the design and application of the transitional phases. Here, based on results from semi‐in situ transmission electron microscopy, density functional theory, and X‐ray photoemission experiments, a physical picture of transitional structures is discovered, in which continuous variations in atomic positions form along a previously unreported anatase‐to‐rutile phase transformation path of [010]A–to–[1¯1¯1$\overline 1 \overline 1 1$]R and (004)A–to– (011)R. These gradient structures give rise to continuous band bending, which promotes electron‐hole separation and inhibits their recombination across the bulk of the particles, leading to a large functionally active volume fraction and resulting in high photoactivity. These findings suggest that interphase matter based on extended gradient structures can be designed to advance new functions not achievable using abrupt interfaces. [ABSTRACT FROM AUTHOR]

(D) TGF 1 promoter-driven mouse TIF1 turned on in the presence of TGF 1 protein at a similar level to cytomegalovirus (CMV) promoter-driven mouse TIF1 , leading to an expression of TIF1 and suppression of fibrosis genes. TGF 1-promoter-driven TIF1 gene therapy significantly reduced liver fibrosis as much as CMV promoter-driven TIF1 gene therapy did (Figure S5A,B). Dear Editor, Recently, we reported the role of transcriptional intermediary factor-1 (TIF1 ) from hepatic stellate cells (HSCs) in preventing liver fibrosis.1 Therefore, an effective strategy to supply I TIF1 i during liver injury offers significant therapeutic promise. (B and C) TGF 1 promoter-driven human TIF1 turned on in the presence of TGF 1 protein, leading to the expression of TIF1 and suppression of fibrosis genes. [Extracted from the article]