China has updated its national guideline recommending antiretroviral therapy (ART) to all people living with HIV (PLWH) since 2016. This study was to investigate the prevalence of behavioral intention to initiate ART among HIV-infected men who have sex with men (MSM) with CD4 levels >350 cells/mm3, who had just become eligible to receive free ART in China. A cross-sectional survey was conducted among 262 eligible HIV-infected MSM who had never received ART. The theory of planned behavior (TPB) was used to guide the variable selection. The prevalence of behavioral intention to initiate ART was 69.9%. After adjusting for significant background variables, all five constructs of TPB were significantly associated with behavioral intention to initiate ART. These significant constructs were: positive attitudes (adjusted odds ratios, AOR: 1.14; 95% CI [1.06, 1.24]) and negative attitudes (AOR: 0.89; 95% CI [0.82, 0.97]) toward immediate ART initiation; perceived their significant others would support them to initiate ART immediately (perceived subjective norm; AOR: 1.14; 95% CI [1.03, 1.25]); perceived high proportion of PLWH having similar CD4 cell levels were on ART (perceived descriptive norm; AOR: 2.22, 95% CI [1.16, 4.24]); and being confident in initiating ART immediately (perceived behavioral control; AOR: 1.21; 95% CI [1.04, 1.39]). Prevalence of behavioral intention to initiate ART was high among this group of MSM. Effective health promotion is needed to translate behavioral intention into related action. TPB may be a useful framework for developing future health promotion increasing ART coverage in this group.

Cardiac hypertrophy has been a high prevalence rate throughout the world. It has posed a big threat to public health due to limited therapeutic approaches. Previous studies showed that pathological cardiac hypertrophy was associated with autophagy, microRNAs (miRNA), and other signaling pathways, while the molecular mechanisms remain incompletely characterized. In this study, we used thoracic aortic constriction (TAC)‐induced mice and angiotensin‐II (Ang‐II)‐induced H9C2 cell line as cardiac hypertrophy model to investigate the role of miR‐26a‐5p in cardiac hypertrophy. We found that miR‐26a‐5p was downregulated in cardiac hypertrophy mice. Overexpression of miR‐26a‐5p by type 9 recombinant adeno‐associated virus (rAAV9) reversed the heart hypertrophic manifestations. The phenotypes were also promoted by miR‐26a‐5p inhibitor in Ang‐II‐induced H9C2 cells. Through miRNA profile analysis and dual‐luciferase reporter assay, ADAM17 was identified as a direct target of miR‐26a‐5p. Restored expression of ADAM17 disrupted the effect of miR‐26a‐5p on cardiac hypertrophy. To sum up, these results indicated that miR‐26a‐5p played an inhibitory role in cardiac hypertrophy and dysfunction via targeting ADAM17. The miR‐26a‐5p‐ADAM17‐cardiac hypertrophy axis provided special insight and a new molecular mechanism for a better understanding of cardiac hypertrophy disease, as well as the diagnostic and therapeutic practice.

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Receptor-interacting protein 3(RIP3), a RIP family member, has been reported as a critical regulator of necroptosis and involves in the pathogenesis of various heart diseases. However, its role in the development of myocardial hypertrophy after pressure overload is unclear. We aimed to investigate the roles of RIP3 in pathological cardiac hypertrophy. A rat model of myocardial hypertrophy induced by the aortic banding method was used in this study. Neonatal rat cardiomyocytes (NRCMs) were stimulated with angiotensin II (Ang-II) or phenylephrine (PE) to induce neurohumoral stress. Our results showed that RIP3 level was significantly elevated in the hypertrophic myocardium tissues from patients, rats subjected to AB surgery, and NRCMs treated with Ang-II or PE. After downregulation of RIP3 expression in NRCMs, the phenotypes of myocardial hypertrophy were obviously alleviated. In mechanism, we demonstrated that RIP3 interacts with mixed lineage kinase domain-like protein (MLKL) and promotes its cell membrane localization to increase the influx of calcium within cells, thereby mediating the development of myocardial hypertrophy. More interestingly, we found the blockage of calcium influx by 2-aminoethoxydiphenyl borate, and lanthanum chloride efficiently reverses RIP3-induced cardiac remodeling in NRCMs. Taken together, our findings indicate a key role of the RIP3-MLKL signaling pathway in myocardial hypertrophy, which may be a novel promising treatment strategy for myocardial hypertrophy.