From global to national: The role of urban agglomerations in China's new development paradigm.

Urban agglomerations (UAs), which serve as pivotal hubs for economic and innovative convergence, play a crucial role in enhancing internal circulation and strengthening external linkages. This study utilizes the China city-level multi-regional input-output tables, incorporating the Dagum Gini coefficient and kernel density estimation methods, to perform a thorough quantitative analysis. Disparities within the national and global value chains ("dual value chains") of Chinese UAs from 2012 to 2017 were assessed. Additionally, the logarithmic mean Divisia index (LMDI) method was applied to disaggregate the drivers of both national and global intermediate inputs (NII and GII). The study's key findings include the following: (1) The national value chain (NVC) within UAs exhibits robust growth, contrasting with the decline in the global value chain (GVC). (2) The inter-UA disparity contribution rate significantly surpasses the combined rates of intra-UA contribution and super-variation density. (3) Distinct evolutionary peak trends are discerned among various UAs within the "dual value chains", highlighting diverse spatial polarization characteristics and expansiveness. (4) The growth of the NVC has transitioned from a negative to a positive impact on NII, while the decline in GVC has substantially counteracted GII growth. Economic and demographic factors notably drive positive improvements in both NII and GII, whereas the efficiency of outflows presents a negative driving effect. Based on these findings, this study offers strategic recommendations to facilitate the effective integration of UAs into the new development paradigm, thereby providing a scientific basis for related decision-making processes.

Salusin-α mitigates diabetic nephropathy via inhibition of the Akt/mTORC1/p70S6K signaling pathway in diabetic rats.

Salusin-α is a bioactive peptide that protects against atherosclerosis and hepatosteatosis. Serum salusin-α level is declined in patients suffering with renal insufficiency. However, it is still undefined whether salusin-α plays a role in diabetic nephropathy. The present study was designed to investigate the potential roles of salusin-α in diabetic renal disease. Herein, we demonstrated that the salusin-α levels in both plasma and kidney tissues from diabetic rats were obviously downregulated. Exogenous administration of salusin-α eliminated the typical characteristics of diabetic nephropathy. Salusin-α treatment decreased renal fibrosis, which was related with reduced epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. Injection of salusin-α suppressed the production of reactive oxygen species (ROS) via attenuation of NADPH oxidase subunits protein expressions and recovery of the antioxidant system. Mechanistically, the activated Akt/mTORC1/p70S6K signaling pathway in diabetic nephropathy was counteracted by salusin-α treatment. Our results demonstrated that salusin-α exerted protective effect against diabetic nephropathy via reduced oxidative stress and fibrosis, dependent on inactivation of the Akt/mTORC1/p70S6K signaling cascade. Salusin-α may be considered as a promising target for the treatment of diabetic nephropathy.

Salusin­ß participates in high glucose­induced HK­2 cell ferroptosis in a Nrf­2­dependent manner.

Ferroptosis is critically involved in the pathophysiology of diabetic nephropathy (DN). As a bioactive peptide, salusin­ß is abundantly expressed in the kidneys. However, it is unclear whether salusin­ß participates in the pathologies of diabetic kidney damage by regulating ferroptosis. The present study found that high glucose (HG) treatment upregulated the protein expressions of salusin­ß in a dose­ and time­dependent manner. Genetic knockdown of salusin­ß retarded, whereas overexpression of salusin­ß aggravated, HG­triggered iron overload, antioxidant capability reduction, massive reactive oxygen species production and lipid peroxidation in HK­2 cells. Mechanistically, salusin­ß inactivated nuclear factor erythroid­derived 2­like 2 (Nrf­2) signaling, thus contributing to HG­induced ferroptosis­related changes in HK­2 cells. Notably, the protein expression of salusin­ß was upregulated by ferroptosis activators, such as erastin, RSL3, FIN56 and buthionine sulfoximine. Pretreatment with ferrostatin­1 (a ferroptosis inhibitor) prevented the upregulated protein expression of salusin­ß in HK­2 cells exposed to HG. Taken together, these results suggested that a positive feedback loop between salusin­ß and ferroptosis primes renal tubular cells for injury in diabetes.