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Fluoride, a ubiquitous environmental compound, carries significant health risks at excessive levels. This study investigated the reproductive toxicity of fluoride exposure during puberty in mice, focusing on its impact on testicular development, spermatogenesis, and underlying mechanisms. The results showed that fluoride exposure during puberty impaired testicular structure, induced germ cell apoptosis, and reduced sperm counts in mice. Additionally, the SOD activity and GSH content were significantly decreased, while MDA content was significantly elevated in the NaF group. Immunohistochemistry showed an increase in the number of cells positive for GRP78, a key ER stress marker. Moreover, qRT-PCR and Western blot analyses confirmed the upregulation of both Grp7 8 mRNA and protein expression, as well as increased mRNA expression of other ER stress-associated genes (Grp94 , chop , Atf6 , Atf4, and Xbp1) and enhanced protein expression of phosphorylated PERK, IRE1α, eIF2α, JNK, XBP-1, ATF-6α, ATF-4, and CHOP. In conclusion, our findings demonstrate that fluoride exposure during puberty impairs testicular structure, induces germ cell apoptosis, and reduces sperm counts in mice. ER stress may participate in testicular cell apoptosis, and contribute to the testicular damage and decreased sperm counts induced by fluoride. Fluoride exposure during puberty induces testicular germ cell apoptosis, impairs testicular structure, and reduces sperm count in mice. ER stress may participate in testicular cell apoptosis via activating JNK and CHOP, ultimately contributing to testicular damage and decreased sperm counts in mice caused by fluoride exposure during puberty. [Display omitted] • Fluoride exposure during puberty impairs testis development in mice. • Fluoride exposure during puberty decreases sperm counts in mice. • Fluoride triggers testicular germ cells apoptosis in mice. • ER stress involves in fluoride-induced testicular germ cells apoptosis. [ABSTRACT FROM AUTHOR]

Background: Diabetic cardiomyopathy (DCM) is one of the serious complications of the accumulated cardiovascular system in the long course of diabetes. To date, there is no effective treatment available for DCM. Circular RNA (circRNA) is a novel r2egulatory RNA that participates in a variety of cardiac pathological processes. However, the regulatory role of circular RNA MAP3K5 (circMAP3K5) in DCM is largely unclear. Methods and Results: Microarray analysis of DCM rats' heart circular RNAs was performed and the highly species‐conserved circRNA mitogen‐activated protein kinase kinase kinase 5 (circMAP3K5) was identified, which participates in DCM processes. High glucose‐provoked cardiotoxicity leads to the up‐regulation of circMAP3K5, which mechanistically contributes to cardiomyocyte cell death. Also, in high glucose‐induced H9c2 cardiomyocytes, the level of apoptosis was significantly increased, as well as the expression of circMAP3K5. In contrast, the depletion of circMAP3K5 could reduce high glucose‐induced apoptosis in cardiomyocytes. In terms of mechanism, circMAP3K5 acts as a miR‐22‐3p sponge and miR‐22‐3p directly target death‐associated protein kinase 2 (DAPK2) in H9c2 cardiomyocytes, where in circMAP3K5 upregulates DAPK2 expression by targeting miR‐22‐3p. Moreover, we also found that miR‐22‐3p inhibitor and pcDNA DAPK2 could antagonize the protective effects brought by the depletion of circMAP3K5. Conclusion: CircMAP3K5 is a highly conserved noncoding RNA that is upregulated during DCM process. We concluded that circMAP3K5 promotes high glucose‐induced cardiomyocyte apoptosis by regulating the miR‐22‐3p/DAPK2 axis. The results of this study highlight a novel and translationally important circMAP3K5‐based therapeutic approach for DCM. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "MiR-181b-5p Downregulates NOVA1 to Suppress Proliferation, Migration and Invasion and Promote Apoptosis in Astrocytoma" published in PLoS ONE. The correction addresses errors in Figure 4 and File S1 of the article. The corrected Figure 4 shows that downregulation of NOVA1 inhibits cell proliferation, migration, and invasion, and promotes apoptosis in vitro. The corrected File S1 contains the correct Figure S1 and S2. The authors of the article are Feng Zhi, Qiang Wang, Danni Deng, Naiyuan Shao, Rong Wang, Lian Xue, Suinuan Wang, Xiwei Xia, and Yilin Yang. [Extracted from the article]