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Myocardial infarction results in extensive cardiomyocyte apoptosis, leading to the formation of noncontractile scar tissue. Given the limited regenerative capacity of adult mammalian cardiomyocytes, direct reprogramming of cardiac fibroblasts (CFs) into cardiomyocytes represents a promising therapeutic strategy for myocardial repair, and small molecule drugs might offer a more attractive alternative to gene editing approaches in terms of safety and clinical feasibility. This study aimed to reprogram rat CFs into cardiomyocytes using a small molecular chemical mixture comprising CHIR99021, Valproic acid, Dorsomorphin, SB431542, and Forskolin. Immunofluorescence analysis revealed a significant increase in the expression of cardiomyocyte‐specific markers, including cardiac troponin T (cTnT), Connexin 43 (Cx43), α‐actinin, and Tbx5. Changes in intracellular calcium ion levels and Ca2+ signal transfer between adjacent cells were monitored using a calcium ion fluorescence probe. mRNA sequencing analysis demonstrated the upregulation of genes associated with cardiac morphogenesis, myocardial differentiation, and muscle fiber contraction during CF differentiation induced by the small‐molecule compounds. Conversely, the expression of fibroblast‐related genes was downregulated. These findings suggest that chemical‐induced cell fate conversion of rat CFs into cardiomyocyte‐like cells is feasible, offering a potential therapeutic solution for myocardial injury. [ABSTRACT FROM AUTHOR]

Fibroblast growth factor (FGF) signaling plays a crucial role in lung development and repair. Fibroblast growth factor 2 (FGF2) can inhibit fibrotic gene expression and suppress the differentiation of pulmonary fibroblasts (PFs) into myofibroblasts in vitro, suggesting that FGF2 is a potential target for inhibiting pulmonary fibrosis. To gain deeper insights into the molecular mechanism underlying FGF2‐mediated regulation of PFs, we performed mRNA sequencing analysis to systematically and globally uncover the regulated genes and biological functions of FGF2 in PFs. Gene Ontology analysis revealed that the differentially expressed genes regulated by FGF2 were enriched in multiple cellular functions including extracellular matrix (ECM) organization, cytoskeleton formation, β‐catenin‐independent Wnt signaling pathway, supramolecular fiber organization, epithelial cell proliferation, and cell adhesion. Gene Set Enrichment Analysis and cellular experiments confirmed that FGF2 can suppress ECM and actin filament organization and increase PFs proliferation. Taken together, these findings indicate that FGF2 acts as an upstream regulator of the inhibition of PFs activation and may play a regulatory role in pulmonary fibrosis. [ABSTRACT FROM AUTHOR]

Ecosystem stability is threatened by multiple global change factors such as drought and elevated nitrogen deposition. Yet, it is still poorly understood whether soil organisms can buffer against such perturbations. Here we focus on arbuscular mycorrhizal fungi (AMF), a common and widespread group of soil fungi. AMF form symbiotic associations with the majority of terrestrial land plants and promote a range of ecosystem services including plant production, diversity and nutrient cycling.We tested whether AMF have the ability to enhance the resistance and resilience of plant communities under soil moisture deficit (hereby drought) and nitrogen deposition. Grassland microcosms with 11 different plant species were established with and without AMF and exposed to elevated nitrogen levels and to an intermittent period of drought.Drought strongly reduced plant productivity and nitrogen cycling, but had limited effects on plant diversity. Nitrogen enrichment reduced plant diversity and increased nitrogen leaching and N2O emissions. The presence of AMF enhanced plant productivity, plant diversity and reduced nitrogen losses. AMF facilitated the resistance of plant productivity and nitrogen cycling to drought and the recovery of the plant community structure back to its pre drought state. Furthermore, AMF also mitigated the adverse effects of nitrogen enrichment on the resistance of multiple ecosystem functions to drought.Synthesis. Our work highlights the integral role of AMF for the stability of ecosystem functioning; AMF are not only able to promote resistance to harsh conditions of global change but also improve resilience by enabling plant communities to recover. These findings underline AMF's insurance capacity to buffer ecosystems against global change. [ABSTRACT FROM AUTHOR]

Global climate change is one of the most pressing conservation challenges; in particular, changes in precipitation regimes have already substantially influenced terrestrial ecosystems. However, the mechanisms influencing precipitation changes on individual plants and the plant communities in desert grasslands have yet to be fully elucidated. We therefore examine the influence of increased precipitation on plant community compositions in the Gurbantunggut Desert, Xinjiang, northwestern China, from 2005 to 2009. We found that growth of all plant species and the community productivities increased markedly with enhanced water input. Cover of ephemeral synusia also significantly increased due to increased precipitation, implying that the role of the ephemeral community for stabilization of sand dunes was strengthened by increased precipitation. The response of plant community compositions to increased precipitation was primarily reflected as changes in plant density, while increased precipitation did not affect plant species richness and the diversity index. Dominant species drove the response of plant density to increasing precipitation during the five‐year study period. However, the relative responses of rare species were stronger than those of the dominant species, thereby potentially driving species turnover with long‐term increased precipitation. This finding improved our understanding of how increased precipitation drives the changes in plant community composition in desert grasslands and will help to better predict changes in the community composition of ephemerals under future global climate change scenarios. [ABSTRACT FROM AUTHOR]

circNOL10 is a circular RNA expressed at low levels in lung cancer, though its functions in lung cancer remain unknown. Here, the function and molecular mechanism of circNOL10 in lung cancer development are investigated using in vitro and in vivo studies, and it is shown that circNOL10 significantly inhibits the development of lung cancer and that circNOL10 expression is co‐regulated by methylation of its parental gene Pre‐NOL10 and by splicing factor epithelial splicing regulatory protein 1 (ESRP1). circNOL10 promotes the expression of transcription factor sex comb on midleg‐like 1 (SCML1) by inhibiting transcription factor ubiquitination and thus also affects regulation of the humanin (HN) polypeptide family by SCML1. circNOL10 also affects mitochondrial function through regulating the humanin polypeptide family and affecting multiple signaling pathways, ultimately inhibiting cell proliferation and cell cycle progression, and promoting the apoptosis of lung cancer cells, thereby inhibiting lung cancer development. This study investigates the functions and molecular mechanisms of circNOL10 in the development of lung cancer and reveals its involvement in the transcriptional regulation of the HN polypeptide family by SCML1. The results also demonstrate the inhibitory effect of HN on lung cancer cells growth. These findings may identify novel targets for the molecular therapy of lung cancer. This study provides new evidence for the molecular mechanism whereby circRNAs may affect transcriptional regulation in lung cancer cells, and also reveals that circNOL10 inhibits lung cancer development by promoting SCLM1‐mediated transcriptional regulation of the humanin (HN) polypeptide family. The results also demonstrate the inhibitory effect of HN on lung cancer growth. [ABSTRACT FROM AUTHOR]