The Renminbi Exchange Rate Reform and the Rebalancing of China's Growth Model

This paper posits that a proper way to estimate the Renminbi(RMB) exchange rate is to base the evaluation on the Balassa-Samuelson effect, and that the optimal way to facilitate China's growth model transformation is gradual RMB internationalization and capital account liberalization. Regression estimates show that the gross domestic product per capita growth rate, or the productivity growth rate, has strong explanatory validity when estimating the RMB exchange rate. The findings further assert that, as the growth of gross fixed capital formation slows, and the growth of household consumption speeds up, China's economic growth will be sustained. The RMB exchange rate regime is one in which gradual reforms must yield to interest rates levels and hence should only be revalued conditionally.

PGAM5-Mediated PHB2 Dephosphorylation Contributes to Diabetic Cardiomyopathy by Disrupting Mitochondrial Quality Surveillance

Disruption of the mitochondrial quality surveillance(MQS)system contributes to mitochondrial dysfunction in diabetic cardiomyopathy(DCM).In this study,we observed that cardiac expression of phosphoglycerate mutase 5(PGAM5),a mitochondrial Ser/Thr protein phosphatase,is upregulated in mice with streptozotocin-induced DCM.Notably,DCM-related cardiac structural and functional deficits were negated in cardiomyocyte-specific Pgam5 knockout(Pgam5^(CKO))mice.Hyperglycemic stress impaired adenosine triphosphate production,reduced respiratory activity,and prolonged mitochondrial permeability transition pore opening in acutely isolated neonatal cardiomyocytes from control Pgam5^(f/f) mice,and these effects were markedly prevented in cardiomyocytes from Pgam5^(CKO) mice.Likewise,three main MQS-governed processes—namely,mitochondrial fission/fusion cycling,mitophagy,and biogenesis—were disrupted by hyperglycemia in Pgam5^(f/f),but not in Pgam5^(CKO),cardiomyocytes.On the basis of bioinformatics prediction of interaction between PGAM5 and prohibitin 2(PHB2),an inner mitochondrial membrane-associated scaffolding protein,co-immunoprecipitation,and immunoblot assays demonstrated that PGAM5 dephosphorylates PHB2 on Ser91.Transfection of cardiomyocytes with phosphodefective or phosphomimetic Ser91 mutants of PHB2 confirmed a critical role for PGAM5-mediated dephosphorylation of PHB2 in mitochondrial dysfunction associated with hyperglycemic stress.Furthermore,knockin mice expressing phosphomimetic PHB2^(S91D) were resistant to diabetes-induced cardiac dysfunction.Our findings highlight the PGAM-PHB2 axis as a novel and critical regulator of mitochondrial dysfunction in DCM.