Cardiovascular diseases (CVDs) remain a major global health challenge, underscoring the need for novel, accessible, and effective therapeutic strategies. This review critically evaluates the phytochemical composition and cardioprotective potential of Passiflora species, summarizes the mechanisms of action of their principal bioactive compounds, and identifies key research gaps hindering clinical translation. With over 500 species distributed worldwide, many Passiflora plants are traditionally used in herbal medicine. Preclinical evidence suggests that compounds such as phenolics, alkaloids, and triterpenoid saponins exert cardioprotective effects through antioxidant and anti-inflammatory activities, vasodilation, blood pressure regulation, endothelial function improvement, and autonomic nervous system modulation. However, these findings are largely based on a limited number of species, often using non-standardized extracts, and lack comprehensive structure-activity relationship (SAR) analyses and clinical validation. Endemic Passiflora species remain underexplored, despite their potential to yield novel compounds with enhanced bioactivity. This review emphasizes the need for extract standardization, robust pharmacokinetic studies, and the integration of omics technologies and molecular modeling to accelerate compound discovery and development. Overall, Passiflora species contain promising bioactive molecules with significant in vitro and in vivo cardioprotective effects. Nonetheless, rigorous and standardized research, including clinical trials, is essential to fully assess their therapeutic value and support their integration into evidence-based cardiovascular care.

Circular RNAs (circRNAs) are primarily produced through pre-mRNA back-splicing, yet their target repertoire and functional mechanisms remain elusive. Here, we present circTargetMap, a computational framework for globally mapping circRNA targets using RNA-RNA interactomes obtained via RNA in situ conformation sequencing (RIC-seq) in the hippocampus and ten human cell lines. This approach identified 117,163 high-confidence circRNA-target RNA interactions, with 83% of target mRNAs bound by multiple circRNAs. Functionally, CDR1as and circRMST repress target mRNA translation by sequestering them into processing bodies (P-bodies)-membraneless granules-through sequence-specific base-pairing, probably independent of AGO2, DICER, and microRNA (miRNAs). To directly capture granule-associated interactions, we developed the granule RIC-seq (GRIC-seq) method, revealing the broad role of circRNA-target RNA interactions in translational repression. Moreover, pathogenic variants are significantly enriched around circRNA-target RNA interaction sites, suggesting potential roles in disease. Our study provides valuable resources for circRNA functional exploration and a framework for investigating RNA-RNA interactions within membraneless organelles.

Thrombosis, the leading cause of death worldwide, involves both platelet activation and coagulation reaction. Astaxanthin (ASX) is a carotenoid with potent antioxidant activity and beneficial effects to the cardiovascular system. This study aims to systematically elucidate the antithrombotic potential of ASX and the underlying mechanisms.

Rats and mice were treated with ASX by gavage to examine the in vivo effects of ASX. Human platelets and liver cells were directly treated with ASX to evaluate its in vitro effects. Network pharmacology and immunoblotting were performed to analyse the targets of ASX. Thrombus components including platelets and fibrin were visualized by specific fluorescent antibodies using intravital microscopy.

ASX treatment led to attenuated platelet aggregation, adhesion, spreading, clot retraction and reduced integrin activation and granule secretion. ASX inhibited reactive oxygen species (ROS) production, and its downstream signalling pathways PI3K/Akt/mTOR and MAPK/ERK during platelet activation. ASX suppressed blood coagulation, both extrinsic and intrinsic, by interfering with hepatic transcription of coagulation factors through reducing hepatic ROS and ROS-responsive hepatocyte nuclear factor 4α (HNF4α). Treatment with ASX in human platelets and liver cells recapitulated the observations in animals. ASX and aspirin comparably inhibited FeCl₃-induced arterial thrombosis and stenosis-induced venous thrombosis. However, unlike aspirin which targets only platelets, ASX inhibited both platelets and fibrin in the cremaster thrombosis model without causing excessive bleeding.

ASX exhibits multiple antithrombotic effects by suppressing platelet- and hepatic-ROS and the downstream responsive pathways. ASX represents a novel strategy for thrombosis prevention.

Abdominal aortic aneurysm (AAA) and major depressive disorder (MDD) are prevalent conditions with substantial global health burdens. Growing clinical evidence indicates a close relationship between them, implicating shared pathogenic mechanisms of immune dysregulation and inflammation. Deciphering this molecular interplay is critical, as it may reveal unified therapeutic strategies for these distinct disorders. This study aims to identify such shared molecular pathways, elucidate their co-pathogenesis, and discover novel therapeutic targets with dual relevance.

We integrated seven gene expression datasets, employing differential expression analysis and weighted gene co-expression network analysis to identify shared modules. Hub genes were prioritized via machine learning and validated using scRNA-seq and murine models.

Integrative analysis revealed 100 shared genes. TBC1D10C was identified as a key hub gene and validated across platforms. Immune infiltration and scRNA-seq analysis localized TBC1D10C primarily to B and CD4⁺ T cells, where its expression inversely correlated with lymphocyte activation. Mouse models of AAA and MDD both exhibited downregulated TBC1D10C.

TBC1D10C is a key regulator in AAA and MDD. Its expression shows a negative correlation with lymphocyte activation and inflammation. This study provides novel insights into their shared immunopathology and nominates a potential therapeutic target.

Abdominal aortic aneurysm (AAA) is a degenerative vascular disease with a high mortality rate of rupture, yet effective pharmacological interventions to delay its progression or prevent rupture remain unavailable. Vascular calcification (VC), a prominent pathological feature of AAA, exhibits a paradoxical role. Clinical and biomechanical studies confirm that VC exerts a dual effect: it accelerates AAA progression by inducing local stress concentration, while simultaneously providing mechanical stability through global load-sharing effect. This functional paradox may stem from a dynamic imbalance between anabolic and catabolic processes at the cellular and molecular levels. Specifically, microcalcification is mediated by the osteogenic transition of vascular smooth muscle cells (VSMCs), whereas the osteoclastic transformation of macrophages contributes to the ultimate matrix degradation. Furthermore, the impacts of vascular aging, sex differences, and metabolic dysregulation between VC and AAA are briefly summarized. This review systematically synthesizes multi-scale evidence to elucidate the dual role of VC in AAA progression, proposing a non-linear dynamic trajectory linking microcalcification initiation to macrocalcification maturation during aneurysm progression. Finally, it also emphasizes that future research should shift from assessing static calcification burden toward dynamically monitoring the metabolic activity of microcalcification, as well as discussing emerging therapeutic targets. This perspective offers new insights for early risk stratification and precise intervention in AAA.

Mesenchymal stem cell (MSC)-based therapy holds significant promise in regenerative medicine, leveraging their multipotent differentiation capacity and paracrine effects. However, clinical translation is limited by poor cell survival and engraftment in a hostile injury microenvironment, where detachment-induced anoikis and insufficient extracellular matrix (ECM) adhesion compromise their therapeutic efficacy. Here, we engineered MSCs with surface-anchored von Willebrand factor A3 domain (vWF A3), a natural collagen-binding domain with exceptional affinity for type I and III collagen, to simultaneously confer collagen-targeting and prosurvival functionalities. The vWF A3-modified MSCs (vWF A3-MSCs) exhibited enhanced collagen-binding capacity, improving retention in myocardial infarction (MI) and osteoarthritis (OA) lesions. Beyond adhesion, vWF A3-MSCs demonstrated improved reparative capacity and anoikis resistance, driven by the activation of ECM-receptor interaction and integrin β3 signaling. These modifications promoted proangiogenic effects via mitogen-activated protein kinase pathway activation while enhancing cell survival through Hippo pathway suppression. In vivo studies confirmed the superior therapeutic efficacy of vWF A3-MSCs in both MI and OA models, highlighting how the artificially constructed collagen-targeting receptors on cell and ECM-adhesion-targeted strategy reprogram cellular fate and enhance therapeutic efficacy in stem cell-based regenerative medicine.

This scoping review was designed to address the core question: In the field of poststroke hand function rehabilitation, what is the current status of technical application, evidence characteristics, and research gaps of robot-assisted therapy in the existing literature? The review aimed to delineate the knowledge landscape of this field, with its unique contributions encompassing the systematic classification of robotic device technical types and their corresponding training paradigms, the identification of key concepts, evidence patterns, and research gaps in current studies, and guiding the design of more targeted future systematic reviews and clinical trials. Following Joanna Briggs Institute guidelines, we searched nine databases (PubMed, Embase, Web of Science, Cochrane Library, CINAHL, CBM, CNKI, Wanfang, VIP) until June 24, 2025. Analysis of 33 studies indicated the following: acute-phase robot-assisted therapy reduced spasticity and pain with functional recovery comparable to conventional therapy; subacute-phase robot-assisted therapy improved motor function and grip strength more effectively; and chronic-phase intent-driven robot-assisted therapy maintained 6-mo Action Research Arm Test gains. Robot-assisted therapy demonstrated favorable safety across phases and may provide clinically meaningful functional benefits. Evidence supports robot-assisted therapy's phase-specific value, warranting future large-scale trials to optimize protocols and explore neuroplasticity mechanisms.

Outpatient intravenous (IV) diuretic treatment is an effective and safe strategy for worsening heart failure (WHF). Still, hospitalization cannot be avoided in a substantial portion of patients and potential predictors of HF hospitalization (HFH) are eagerly awaited.

We aimed to identify predictors of HFH after outpatient IV diuretic treatment for WHF, in order to improve the selection of patients who qualify for successful outpatient IV diuretic treatment.

We studied WHF patients receiving intravenous diuretics in an outpatient day-care setting in one of two Dutch hospitals. A total of 366 patients from hospital A were used to identify predictors of 30-day HF (re-)hospitalization (HFH), which occurred in 88 (24.0%). Mean age was 76 years, 57% were male and 49% had ejection fraction below 40%. Age, eGFR, NT-proBNP, sodium, and haemoglobin were identified as predictors of HFH. The multivariable logistic regression model containing these factors had acceptable calibration and discrimination (AUC 0.73). The performance of the model was less favorable in the 127 patients from hospital B (29 patients with 30-day HFH), with AUC 0.65 and suboptimal calibration, indicating overestimation of risk. Doubling of NT-proBNP plasma levels and higher ambulatory oral loop diuretic dosages were strong predictors of mortality and HFH at 6 months in hospital A.

In patients with WHF receiving outpatient day-care intravenous diuretic treatment, age, eGFR, NT-proBNP, sodium and haemoglobin predicted 30-day HFH. These factors may guide decisions on day-care treatment versus hospitalization, but require further validation Fig 2.

Cardiac hypertrophy is a prevalent adaptive response to hemodynamic and neurohormonal stress, but its persistence often leads to maladaptive remodeling and heart failure. This review integrates recent advances in the molecular regulation of hypertrophy, encompassing classical signaling cascades-including phosphoinositide 3-kinase (PI3K)-Ak strain transforming (Akt)-mammalian target of rapamycin (mTOR), mitogen-activated protein kinases (MAPKs), G protein-coupled receptors (GPCRs), AMP-activated protein kinase (AMPK), Hippopotamus-Yes-associated protein (Hippo-YAP), and Wingless-related integration site/Beta-catenin (Wnt/β-catenin) pathways-alongside metabolic reprogramming, epigenetic control, and organelle dynamics. Recent findings emphasize the role of transcriptional and post-transcriptional regulation, mitochondrial quality control, and post-translational modifications in modulating cardiomyocyte structure and function. One of the special focuses is on the gut-heart axis, emphasizing the emerging role of the gut microbiota as a pivotal systemic regulator of cardiac remodeling. While significant strides have been made in delineating the molecular underpinnings of cardiac hypertrophy, critical gaps remain in early detection, mechanistic specificity, and therapeutic translation. Moving forward, integrative, multi-omics approaches and improved experimental models will be essential to unravel the complexity of hypertrophic signaling networks. Based on the current evidence, a detailed understanding of the molecular regulation of cardiac hypertrophy may ultimately enable the development of targeted interventions to prevent or reverse pathological remodeling of cardiac hypertrophy related to heart failure.

Depression and anxiety are common, disabling conditions that often require sustained psychiatric care. While digital mental health interventions (DMHIs) offer scalable access, few integrate measurement-based care (MBC) to track outcomes such as minimal clinically important difference (MCID) and remission. The purpose of this study was to evaluate the rate and timing of MCID and remission in depression and anxiety among patients with elevated baseline depression and anxiety scores receiving psychiatry services through Rula Health, a MBC-based DMHI that connects patients with psychiatric care. Symptoms were assessed prior to psychiatric visits over a 24-week period and used to evaluate effect sizes, as well as rates of MCID and remission. Kaplan-Meier and Cox proportional hazards models were used to estimate the timing of MCID and remission, and to identify demographic and clinical factors associated with achieving each outcome. A total of 7124 adults with elevated depression symptoms and 7628 with elevated anxiety symptoms at baseline were included. Depression and anxiety symptoms decreased with large effect sizes (d's = -1.17 to -1.62). The median survival time to MCID in depression was 12 weeks and remission 22 weeks. The median survival time to MCID in anxiety was 11 weeks and remission 19 weeks. Several demographic and clinical characteristics were associated with time to MCID and remission. MBC-based digital psychiatry services can support sustained, clinically meaningful change. Faster improvement among patients with varying clinical and demographic characteristics highlights Rula Health's ability to address a range of patient needs.