Lake biodiversity is an incomplete indicator of exogenous forcing insofar as it ignores underlying deformations of community structure. Here, we seek a proxy for deformation in a network of diatom assemblages comprising 452 species in 273 lakes across China. We test predictions from network theory that nodes of similar type will tend to self‐organize in an unstressed system to a positively skewed frequency distribution of nodal degree. The empirical data reveal shifts in the frequency distributions of species associations across regions, from positive skew in lakes in west China with a history of low human impacts, to predominantly negative skew amongst lakes in highly disturbed regions in east China. Skew values relate strongly to nutrient loading from agricultural activity and urbanization, as measured by total phosphorus in lake water. Reconstructions through time show that positive skew reduces with temporal intensification of human impacts in the lake and surrounding catchments, and rises as lakes recover from disturbance. Our study illustrates how network parameters can track the loss of aquatic assemblage structure in lakes associated with human pressures.

The south-east margin of Tibet is highly sensitive to global environmental change pressures, in particular, high contemporary reactive nitrogen (Nr) deposition rates (ca. 40 kg ha(-1)  yr(-1) ), but the extent and timescale of recent ecological change is not well prescribed. Multiproxy analyses (diatoms, pigments and geochemistry) of (210) Pb-dated sediment cores from two alpine lakes in Sichuan were used to assess whether they have undergone ecological change comparable to those in Europe and North America over the last two centuries. The study lakes have contrasting catchment-to-lake ratios and vegetation cover: Shade Co has a relatively larger catchment and denser alpine shrub than Moon Lake. Both lakes exhibited unambiguous increasing production since the late 19th to early 20th. Principle component analysis was used to summarize the trends of diatom and pigment data after the little ice age (LIA). There was strong linear change in biological proxies at both lakes, which were not consistent with regional temperature, suggesting that climate is not the primary driver of ecological change. The multiproxy analysis indicated an indirect ecological response to Nr deposition at Shade Co mediated through catchment processes since ca. 1930, while ecological change at Moon Lake started earlier (ca. 1880) and was more directly related to Nr deposition (depleted δ(15) N). The only pronounced climate effect was evidenced by changes during the LIA when photoautotrophic groups shifted dramatically at Shade Co (a 4-fold increase in lutein concentration) and planktonic diatom abundance declined at both sites because of longer ice cover. The substantial increases in aquatic production over the last ca. 100 years required a substantial nutrient subsidy and the geochemical data point to a major role for Nr deposition although dust cannot be excluded. The study also highlights the importance of lake and catchment morphology for determining the response of alpine lakes to recent global environmental forcing.

Cardiac fibrosis is a common pathological feature of many cardiovascular diseases. The regulatory mechanisms of miRNAs in cardiac fibrosis are still unknown. Previous studies on miR-214-3p in cardiac fibroblasts reached contradictory conclusions. Thus the role of miR-214-3p in cardiac fibrosis deserves further exploration. Using a combination of in vitro and in vivo studies, we identified miR-214-3p as an important regulator of cardiac fibrosis, and the proliferation and activation of cardiac fibroblasts. We demonstrated that the expression of miR-214-3p is down-regulated in TGF-β1-treated myofibroblasts and transverse aortic constriction (TAC)-induced murine model. Additionally, miR-214-3pflox/flox/FSP1-cre mice and miR-214-3pwt/wt/FSP1-cre mice were subjected to TAC operation or sham operation, and the conditional knockout of miR-214-3p in cardiac fibroblasts aggravates TAC-induced cardiac fibrosis. In vitro, our results indicate that miR-214-3p is an important repressor for fibroblasts proliferation and fibroblast-to-myofibroblast transition by functionally targeting NOD-like receptor family CARD domain containing 5 (NLRC5). In conclusion, our findings show that the deficiency of miR-214-3p exacerbates cardiac fibrosis and reveal a novel miR-214-3p/NLRC5 axis in the regulation of cardiac fibrosis.