Immune and inflammatory responses have an important function in the pathophysiology of pulmonary hypertension (PH). However, little is known about the immune landscape in peripheral circulation in patients with high-altitude pulmonary hypertension (HAPH). We apply single-cell transcriptomics to characterize the monocytes that are significantly enriched in the peripheral blood mononuclear cells (PBMC) of HAPH patients. We discover an increase in C1 (non-classical) and C2 (intermediate) monocytes in PBMCs and a decrease in hypoxia-inducible transcription factor-1α (HIF-1α) in all monocyte subsets associated with HAPH. In addition, we demonstrate that similar immune adaptations may exist in HAPH and PH. Overall, we characterize an immune cell atlas of the peripheral blood in HAPH patients. Our data provide evidence that specific monocyte subsets and HIF-1α downregulation might be implicated in the pathogenesis of HAPH.

Retinal vessels play a pivotal role as biomarkers in the detection of retinal diseases, including hypertensive retinopathy. The manual identification of these retinal vessels is both resource-intensive and time-consuming. The fidelity of vessel segmentation in automated methods directly depends on the fundus images' quality. In instances of sub-optimal image quality, applying deep learning-based methodologies emerges as a more effective approach for precise segmentation. We propose a heterogeneous neural network combining the benefit of local semantic information extraction of convolutional neural network and long-range spatial features mining of transformer network structures. Such cross-attention network structure boosts the model's ability to tackle vessel structures in the retinal images. Experiments on four publicly available datasets demonstrate our model's superior performance on vessel segmentation and the big potential of hypertensive retinopathy quantification.

This study aimed to define the relationship between pulse pressure (PP) and coronary artery calcification (CAC), a proven surrogate marker for coronary heart disease. A total of 170 participants 50–70 years of age from 11 villages of Yunnan Province of China were enrolled randomly into this study. They were examined routinely for diastolic and systolic blood pressure, PP, and CAC. The average PP in the CAC-positive group was significantly higher than that in the CAC-negative group. In the positive CAC group, there were significantly positive correlations between PP and CAC score, volume, mass, as well as density. The area under the receiver operating characteristic curve analysis showed that PP performed well in predicting CAC. In conclusion, among the rural people of southwest of China, PP correlates positively with the coronary calcium Agatston score, volume, mass, and density. PP predicted CAC as well as Framingham Risk Score. The measurement of PP widening may serve as an alternative and convenient method for assessing CAC risk in rural populations with poor accessibility and economic disadvantage over coronary computed tomography scanning. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0/

Both hypertension and sleep disturbance have been closely linked to inflammation. However, the specific role of inflammation in the relationship between sleep disturbance and hypertension remains unclear. We investigated the pairwise associations among a novel inflammatory marker (systemic immune inflammation index ), sleep disturbance, and hypertension in a powerful, racially diverse sample (n = 23,414) from the 2005–2020 National Health and Nutrition Examination Survey (NHANES). We found that participants with high blood pressure and/or sleep disorders had higher levels of Systemic Immune-Inflammatory Index (SII) than those without hypertension or sleep disorders.SII slightly but significantly mediated the relationship between sleep disturbance and hypertension in males but not in females, after adjusting for all covariates (proportion mediate [PM], 1.36%; total effect [TE], 0.0931; direct effect [ADE], 0.0917; verage causal mediation effects [ACME] = 0.0013 [95% CI = 0.0004–0.0024], p = 0.002, in males. Our research showed that SII, sleep disturbance, and hypertension are related. Increased SII levels slightly mediated the association between sleep disturbance and hypertension.

Myocardial ischemia-reperfusion (MI/R) injury frequently occurs during the clinical management of ischemic heart disease. The underlying mechanism includes neutrophil infiltration, heightened intracellular Ca²⁺ levels, mitochondrial energy metabolism disorder. This study investigated the pathological role of the inositol 1,4,5-trisphosphate receptor/mitochondrial calcium uniporter (ITPR1/MCU) pathway in regulating disturbances in intracellular calcium ([Ca²⁺]_i) and mitochondrial calcium ([Ca²⁺]_m) levels during MI/R injury. Furthermore, the study explored the potential of 2-aminoethoxydiphenylborane (2-APB) as a cardioprotective agent against MI/R injury. The outcomes of this investigation demonstrated that the ITPR1/MCU pathway was activated after MI/R, leading to [Ca²⁺]_i/[Ca²⁺]_m overload, impairing mitochondrial structure and function, and promoting cardiomyocyte death. The administered treatment attenuates myocardial injury after MI/R by reversing the [Ca²⁺]_i/[Ca²⁺]_m imbalance, maintaining cardiomyocyte mitochondrial homeostasis and promoting cardiomyocyte survival. Furthermore, the administration of 2-APB exerted a suppressive effect on MCU expression. Notably, the activation of MCU abolished the cardioprotective impact mediated by 2-APB. These results suggest that 2-APB intervenes [Ca²⁺]_i/[Ca²⁺]_m balance and maintains mitochondrial function through the ITPR1/MCU pathway. The strategic manipulation of this pathway holds promise as a prospective avenue for the clinical treatment of MI/R injury.

Atrial fibrillation (AF), the most prevalent clinical atrial arrhythmia, arises from complex dysregulation of multicellular signalling pathways and molecular networks. Recent advances in cardiac electrophysiology have identified the atrial-specific gap junction protein Connexin 40 (Cx40) as a pivotal regulator of intercellular communication and cardiac electrical synchronization in AF pathogenesis. Aberrant Cx40 expression significantly disrupts atrial electrical conduction, yet its precise regulatory mechanisms remain incompletely understood. This review systematically examines the multifaceted roles of Cx40 in AF development, particularly focusing on how Cx40 genetic polymorphisms influence cardiac electrophysiology and promote atrial structural remodelling. Furthermore, we elucidate the ubiquitination-mediated protein degradation pathways governing Cx40 stability. These insights advance our understanding of AF pathophysiology and highlight potential therapeutic targets for precision arrhythmia management.