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Background Antisense long noncoding RNAs (lncRNAs) are single‐stranded RNAs that overlapped gene‐coding regions on the opposite DNA strand and play as critical regulators in cardiovascular diseases. The high conservation and stability may be good advantages for antisense lncRNAs. However, the roles of antisense lncRNAs in cardiomyocyte proliferation and cardiac regeneration are still unknown. Methods and Results In this study, we found that Silent information regulator factor 2 related enzyme 1 (Sirt1) antisense lncRNA expression was significantly increased during heart development. By gain and loss function of Sirt1 antisense lncRNA using adenovirus and locked nucleic acid, respectively, we demonstrated that Sirt1 antisense lncRNA promoted cardiomyocyte proliferation in vitro and in vivo, and the suppression of Sirt1 antisense lncRNA inhibited cardiomyocyte proliferation. Moreover, overexpression of Sirt1 antisense lncRNA enhanced cardiomyocyte proliferation, attenuated cardiomyocyte apoptosis, improved cardiac function, and decreased mortality rate after myocardial infarction. Furthermore, Sirt1 antisense lncRNA can bind the Sirt1 3′‐untranslated region, enhancing the stability of Sirt1 and increasing Sirt1 abundance at both the mRNA and protein levels. Finally, we found that Sirt1 was involved in Sirt1 antisense lncRNA‐induced cardiomyocyte proliferation. Conclusions The present study identified Sirt1 antisense lncRNA as a novel regulator of cardiomyocyte proliferation and cardiac regeneration by interacting and stabilizing Sirt1 mRNA, which may serve as an effective gene target for preventing myocardial infarction.

Abstract Assessing the effectiveness of vegetation restoration along the Yangtze River shoreline and exploring its relationship with land use changes are imperative for providing recommendations for sustainable management and environmental protection. However, the impact of vegetation restoration post-implementation of the Yangtze River Conservation Project remains uncertain. In this study, utilizing Sentinel-2 satellite imagery and Dynamic World land use data from pre- (2016) and post- (2022) Yangtze River Conservation Project periods, pixel-based binary models, transition matrices, and geographically weighted regression models were employed to analyze the status and evolution of vegetation coverage along the Yangtze River shoreline. The results indicated that there had been an increase in the area covered by high and high-medium vegetation levels. The proportion of vegetation cover shifting to better was 4201.87 km2 (35.68%). Hotspots of vegetation coverage improvement were predominantly located along the Yangtze River. Moreover, areas witnessing enhanced vegetation coverage experienced notable land use changes, notably the conversion of water to crops (126.93 km2, 22.79%), trees to crops (59.93 km2, 10.76%), and crops to built area (59.93 km2, 10.76%). Notably, the conversion between crops and built area emerged as a significant factor influencing vegetation coverage improvement, with average regression coefficients of 0.68 and 0.50, respectively. These outcomes underscore the significance of this study in guiding ecological environmental protection and sustainable management along the Yangtze River shoreline.

Objectives: In order to compare and rank the most effective acupuncture therapy for primary dysmenorrhea and provide evidence-based medical support for clinical treatment of this disease. Methods: A comprehensive search was conducted on China National Knowledge Infrastructure (CNKI), Wanfang Database, Information Chinese Journal Service Platform (VIP), China Biomedical Literature Service System (SinoMed), PubMed, Web of Science, Embase, and Cochrane Library databases from their inception to May 1, 2023. The Cochrane Collaboration Risk of Bias Tool was used to evaluate bias risk, and the GeMTC package of Stata 15.1 software and R 4.3.1 software was used to perform network Meta-analysis. Results: 70 studies were included, including 5772 patients with primary dysmenorrhea, involving 25 kinds of acupuncture techniques commonly used in clinic. The quality of the included literature was low, most of them did not mention the registration information of clinical trial centers, and the specific sample size estimation method was unclear. Some literature did not explain the specific random method, distribution concealment and blindness, so there was a certain publication bias and small sample effect. Results showed that for improving the clinical effective rate, the top three treatments were salt-separated moxibustion, massotherapy + acupoint patching, acupuncture + heat-sensitive moxibustion. In terms of reducing the visual analogue scale(VAS), the top three treatments were massotherapy + acupoint patching, acupuncture + acupoint patching and warm acupuncture. In terms of alleviating cox menstrual symptom scale (CMSS), the top three treatments were acupuncture + acupoint patching, acupoint patching and point embedding. In relieving TCM symptom score, the top three treatments were acupoint patching + heat-sensitive moxibustion, acupoint patching and moxibustion. Conclusion: Different acupuncture therapies have more advantages than oral analgesics in improving the clinical effective rate, reducing VAS score, reducing CMSS score, and alleviating TCM symptom score. Among them, massage therapy + acupoint patching, acupuncture + acupoint patching and acupoint patching may be the best solutions for the treatment of primary dysmenorrhea. However, more large-sample, multi-center and high-quality randomized controlled trials are needed to demonstrate.

The long non-coding RNA (lncRNA) PTENP1 is a pseudogene of phosphatase and tensin homologue deleted on chromosome ten (PTEN), has been implicated in smooth muscle cell (SMC) proliferation and apoptosis. PTENP1 is the pseudogene of PTEN. However, it is unclear whether and how PTENP1 functions in the proliferation and apoptosis of human aortic SMCs (HASMCs). Here, we hypothesised that PTENP1 inhibits HASMC proliferation and enhances apoptosis by promoting PTEN expression. PCR analysis and Western blot assays respectively showed that both PTENP1 and PTEN were up-regulated in human aortic dissection (AD) samples. PTENP1 overexpression significantly increased the protein expression of PTEN, promoted apoptosis and inhibited the proliferation of HASMCs. PTENP1 silencing exhibited the opposite effects and mitigated H2O2-induced apoptosis of HASMCs. In an angiotensin II (Ang II)-induced mouse aortic aneurysm (AA) model, PTENP1 overexpression potentiated aortic SMC apoptosis, exacerbated aneurysm formation. Mechanistically, RNA pull-down assay and a series of luciferase reporter assays using miR-21 mimics or inhibitors identified PTENP1 as amolecular sponge for miR-21 to endogenously compete for the binding between miR-21 and the PTEN transcript, releasing PTEN expression. This finding was further supported by in vitro immunofluorescent evidence showing decreased cell apoptosis upon miR-21 mimic administration under baseline PTENP1 overexpression. Ex vivo rescue of PTEN significantly mitigated the SMC apoptosis induced by PTENP1 overexpression. Finally, Western blot assays showed substantially reduced Akt phosphorylation and cyclin D1 and cyclin E levels with up-regulated PTENP1 in HASMCs. Our study identified PTENP1 as a mediator of HASMC homeostasis and suggests that PTENP1 is a potential target in AD or AA intervention. [ABSTRACT FROM AUTHOR]

MiRNAs regulate the cardiomyocyte (CM) cell cycle at the post-transcriptional level, affect cell proliferation, and intervene in harmed CM repair post-injury. The present study was undertaken to characterize the role of let-7i-5p in the processes of CM cell cycle and proliferation and to reveal the mechanisms thereof. In the present study, we used real-time qPCR (RT-qPCR) to determine the up-regulated let-7i-5p in CMs during the postnatal switch from proliferation to terminal differentiation and further validated the role of let-7i-5p by lossand gain-of-function of let-7i-5p in CMs in vitro and in vivo. We found that the overexpression of let-7i-5p inhibited CMproliferation, whereas the suppression of let-7i-5p significantly facilitated CM proliferation. E2F2 and CCND2 were identified as the targets of let-7i-5p, mediating its effect in regulating the cell cycle of CMs. Supperession of let-7i-5p promoted the recovery of heart function post-myocardial infarction by enhancing E2F2 and CCND2. Collectively, our results revealed that let-7i-5p is involved in the regulation of the CM cell cycle and further impacts proliferation, which may offer a new potential therapeutic strategy for cardiac repair after ischemic injury. [ABSTRACT FROM AUTHOR]