Accelerating sea-level rise and decreasing riverine sediment supply are widely considered to lead to global losses of deltaic marshes and their valuable ecosystem services. However, little is known about the degree to which the related erosion of the seaward delta front can provide sediments to sustain salt marshes. Here, we present data from the mesomacrotidal Yangtze Delta demonstrating that marshes have continued to accrete vertically and laterally, despite rapid relative sea-level rise ($10 mm yr −1) and a > 70% decrease in the Yangtze River sediment supply. Marsh progradation has decelerated at a lower rate than fluvial sediment reduction, suggesting an additional source of sediment. We find that under favorable conditions (e.g., a mesomacrotidal range, strong tidal flow, flood dominance, sedimentary settling lag/scour lag effects, and increasing high-tide level), delta-front erosion can actually supply sediment to marshes, thereby maintaining marsh accretion rates in balance with relative sea-level rise. Comparison of global deltas illustrates that the ability of sediment remobilization to sustain marshes depends on coastal processes and varies by more than an order of magnitude among the world's major deltas. Salt marshes are among the world's most valuable ecosystems (Costanza et al. 1997). They sequester carbon, protect shorelines from storm impacts, transform nutrients, contribute to fisheries production, and maintain biodiversity (Barbier et al. 2011; Kirwan and Megonigal 2013; Temmerman et al. 2013; Möller et al. 2014). Unfortunately, many salt marshes have disappeared due to reclamation and waste disposal during the past century (Gedan et al. 2009; Ma et al. 2014). Deltaic marshes are one of the most dynamic landscapes on Earth's surface (Wagner et al. 2017) and are threatened by accelerating sea-level rise and decreases in fluvial sediment supply. Decreasing fluvial sediment supply reduces the ability of salt marshes to accumulate sediments and to build up their soil elevation in balance with the rising sea level (Kirwan et al. 2010; Weston 2014). Although the morphology and evolution of deltas are influenced by various factors (Paola et al. 2011), such as riverine water and sediment discharges (Besset et al. 2019), sediment properties (Caldwell and Edmonds 2014), flow patterns (Shaw et al. 2016), vegetation height and density (Nardin et al. 2016), marine hydrodynamics (waves, tides, and longshore currents) (Caldwell and Edmonds 2014; Besset et al. 2017), land subsidence and sea-level changes (Jerolmack 2009; Syvitski et al. 2009), changes in the fluvial sediment supply and relative sea level are usually the most important for the long-term morphological evolution of deltaic marshes. The rate of global mean sea-level rise increased from 1.

The aim of the present study is to explore the molecular mechanism of fibroblast growth factor 21 (FGF21) in protecting against diabetic cardiomyopathy (DCM). Streptozotocin/high-fat diet (STZ/HFD) was used to induced diabetes in FGF21-deficient mice and their wild-type littermates, followed by evaluation of the difference in DCM between the two genotypes. Primary cultured cardiomyocytes were also used to explore the potential molecular mechanism of FGF21 in the protection of high glucose (HG)-induced cardiomyocyte injury. STZ/HFD-induced cardiomyopathy was exacerbated in FGF21 knockout mice, which was accompanied by a significant reduction in cardiac AMP-activated protein kinase (AMPK) activity and paraoxonase 1 (PON1) expression. By contrast, adeno-associated virus (AAV)-mediated overexpression of FGF21 in STZ/HFD-induced diabetic mice significantly enhanced cardiac AMPK activity, PON1 expression and its biological activity, resulting in alleviated DCM. In cultured cardiomyocytes, treatment with recombinant mouse FGF21 (rmFGF21) counteracted HG-induced oxidative stress, mitochondrial dysfunction, and inflammatory responses, leading to increased AMPK activity and PON1 expression. However, these beneficial effects of FGF21 were markedly weakened by genetic blockage of AMPK or PON1. Furthermore, inactivation of AMPK also markedly blunted FGF21-induced PON1 expression but significantly increased HG-induced cytotoxicity in cardiomyocytes, the latter of which was largely reversed by adenovirus-mediated PON1 overexpression. These findings suggest that FGF21 ameliorates DCM in part by activation of the AMPK-PON1 axis.

Fibroblast growth factor 21 (FGF21) is important in glucose, lipid homeostasis and insulin sensitivity. However, it remains unknown whether FGF21 is involved in insulin expression and secretion that are dysregulated in type 2 diabetes mellitus (T2DM). In this study, we found that FGF21 was down‐regulated in pancreatic islets of db/db mice, a mouse model of T2DM, along with decreased insulin expression, suggesting the possible involvement of FGF21 in maintaining insulin homeostasis and islet β‐cell function. Importantly, FGF21 knockout exacerbated palmitate‐induced islet β‐cell failure and suppression of glucose‐stimulated insulin secretion (GSIS). Pancreatic FGF21 overexpression significantly increased insulin expression, enhanced GSIS, improved islet morphology and reduced β‐cell apoptosis in db/db mice. Mechanistically, FGF21 promoted expression of insulin gene transcription factors and soluble N‐ethylmaleimide‐sensitive factor attachment protein receptor (SNARE) proteins, the major regulators of insulin secretion, as well as activating phosphatidylinositol 3‐kinase (PI3K)/Akt signaling in islets of db/db mice. In addition, pharmaceutical inhibition of PI3K/Akt signaling effectively suppressed FGF21‐induced expression of insulin gene transcription factors and SNARE proteins, suggesting an essential role of PI3K/Akt signaling in FGF21‐induced insulin expression and secretion. Taken together, our results demonstrate a protective role of pancreatic FGF21 in T2DM mice through inducing PI3K/Akt signaling‐dependent insulin expression and secretion.

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Chemokine C-X-C ligand 16 (CXCL16), a single-pass Type I membrane protein belonging to the CXC chemokine family, is related to the inflammatory response in liver injury. In present study, we investigated the pathophysiological role of CXCL16, a unique membrane-bound chemokine, in acetaminophen (APAP)-induced hepatotoxicity in mice. Mice were injected with APAP, and blood and tissue samples were harvested at different time points. The serum high-mobility group box 1 and CXCL16 levels were quantified by sandwich immunoassays. The liver tissue sections were stained with hematoxylin-eosin or with dihydroethidium staining. The expressions of CXCL16 and other cytokines were examined by real-time polymerase chain reaction. Ly6-B, p-jun N-terminal kinase (p-JNK), and JNK expressions were measured by western blot analysis. Intracellular glutathione, reactive oxygen species, and malondialdehyde levels were also measured. APAP overdose increased hepatic CXCL16 mRNA and serum CXCL16 protein levels. CXCL16-deficient mice exhibited significantly less liver injury and hepatic necrosis, as well as a lower mortality than wild-type (WT) mice in response to APAP-overdose treatment. APAP elevated the production of oxidative stress and decreased mitochondrial respiratory chain activation in WT mice, which was strongly reversed in CXCL16-knockout mice. In addition, CXCL16 deficiency inhibited the neutrophil infiltration and the production of proinflammatory cytokines triggered by APAP-overdose treatment. Our study revealed that CXCL16 is a critical regulator of liver immune response to APAP-induced hepatotoxicity, thus providing a potential strategy for the treatment of drug-induced acute liver failure by targeting CXCL16.