Panvascular aging is characterized by a systemic decline in vascular integrity that underlies the pathogenesis of multiple age-related diseases. Rather than affecting isolated vascular beds, aging triggers widespread changes across the entire circulatory system, including both large vessels and microcirculation in multiple organs. Core mechanisms encompass endothelial dysfunction, glycocalyx degradation, oxidative stress, inflammaging, and disturbed mechanotransduction, which converge to impair vascular homeostasis. At the cellular level, telomere shortening, epigenetic remodeling, and vascular smooth muscle cell phenotypic switching accelerate senescence and extracellular matrix stiffening. Importantly, panvascular aging propagates through systemic inter-organ axes, such as the brain-vascular and heart-kidney networks, thereby amplifying shared pathogenic pathways and promoting organ dysfunction. Consequently, it constitutes an integrative framework linking cardiovascular disease, diabetes, chronic kidney disease, and neurodegeneration. Recognizing panvascular aging as a common pathophysiological axis underscores the importance of developing systemic strategies that enhance vascular resilience beyond singular disease-oriented approaches. Emerging therapeutic strategies - including senotherapeutics, epigenetic modulators, glycocalyx restoration, and metabolic restoration - are being explored as promising interventions to attenuate vascular aging and mitigate multimorbidity. This review synthesizes current insights into the molecular and mechanobiological mechanisms of panvascular aging and frames it as a conceptual keystone in aging biology, highlighting translational opportunities for the prevention and treatment of chronic age-related diseases.
Aim: Pulsed field ablation (PFA) has emerged as a promising strategy for catheter ablation of atrial fibrillation (AF). This study compared perioperative outcomes of pulmonary vein isolation (PVI) performed using robotic magnetic navigation (RMN), cryoballoon (CRYO) ablation, and PFA. Methods: This retrospective study included patients with AF who underwent PVI using RMN ablation (RMN group, n = 112), CRYO ablation (CRYO group, n = 189), or PFA (PFA group, n = 50). Procedural characteristics, perioperative complications, and postoperative recovery were analyzed. Results: Total procedure time was longer in the PFA group than in the CRYO group but shorter than in the RMN group (123.9 ± 14.0 vs. 98.3 ± 14.3 vs. 147.9 ± 19.3 min, P < 0.001). However, left atrial procedure time was shortest in the PFA group (26.6 ± 6.4 vs. 44.7 ± 12.1 vs. 95.1 ± 20.5 min, P < 0.001). Fluoroscopy time was comparable between the PFA and CRYO groups, and significantly shorter in the RMN group (15.2 ± 3.0 vs. 15.0 ± 3.1 vs. 7.4 ± 2.5 min, P < 0.001). Although acute procedural success was comparable across groups, first-pass PVI was achieved more frequently with PFA than with CRYO or RMN {50/50 [100%] vs. 170/189 [89.9%] vs. 100/112 [89.3%], P = 0.030}. The overall incidence of perioperative complications did not differ significantly among the three groups. Conclusion: PFA demonstrated acute safety and efficacy comparable to those of RMN and CRYO ablation for AF, while offering shorter left atrial procedure time and a higher rate of first-pass isolation.
Pulmonary hypertension (PH) is a progressive and life-threatening disorder characterized by elevated pulmonary arterial pressure, vascular remodeling, and right ventricular failure. While the pathogenesis of PH involves endothelial dysfunction, inflammation, and excessive extracellular matrix (ECM) deposition, emerging evidence highlights the pivotal role of integrin-mediated signaling in driving vascular cell behavior and tissue stiffness. Integrins, a family of heterodimeric transmembrane receptors, serve as critical mechanosensors and signal transducers between cells and the ECM. The dysregulation of integrins has been confirmed to promote pathological vascular remodeling through the following mechanisms: (1) Activating focal adhesion kinase (FAK) and Src family kinases, driving excessive proliferation and resistance to apoptosis of pulmonary artery smooth muscle cells; (2) Enhanced transforming growth factor-beta (TGF-β) signaling leads to the transformation of fibroblasts into myofibroblasts and excessive collagen deposition; (3) Ras homolog gene family, member A/Rho-associated protein kinase-mediated cytoskeletal recombination disrupts the integrity of the endothelial barrier, exacerbating inflammation and thrombosis. These pathways collectively increase vascular hardness and maintain a pro-remodeling microenvironment of pulmonary vessels. This review summarizes the current understanding of integrin signaling pathways in PH, with a focus on αvβ3, α5β1, and β1-containing integrins, their downstream effectors (e.g., FAK, TGF-β), and their interplay with inflammatory and fibrotic processes. We also discuss preclinical and clinical evidence supporting integrin-targeted therapies, including Myocardin-related transcription factor 1 and Cilengitide, as potential strategies for modulating vascular remodeling in PH. However, their clinical transformation remains challenged by limited efficacy, context-dependent signaling, and safety concerns. A deeper understanding of integrin biology may facilitate the development of more precise and effective therapeutic strategies for PH.
Aim: Atrial fibrillation and atrial flutter (AF/AFL) represent a growing public health challenge in China amid rapid population aging. This study aimed to comprehensively assess long-term trends, sex- and age-specific patterns, driving factors, and future projections of AF/AFL burden in China from 1990 to 2023. Methods: Data were obtained from Global Burden of Disease 2023. Temporal trends, driving factors, and future projections were evaluated using joinpoint regression, age-period-cohort models, decomposition analysis, frontier analysis, and autoregressive integrated moving average (ARIMA) models. Results: From 1990 to 2023, the absolute numbers of AF/AFL cases, deaths, and disability-adjusted life years (DALYs) increased substantially in China, whereas age-standardized mortality and DALY rates declined overall, with a recent upturn after 2020. Incidence and prevalence were generally higher in males, whereas females had higher mortality and DALYs at older ages. Population aging was the dominant contributor to increases in incidence, prevalence, mortality, and DALYs. Age-period-cohort models analyses showed that among individuals born after 1944, the burden of AF/AFL was higher in males than in females. Frontier analysis indicated that China still lags behind several high Socio-demographic Index regions in AF/AFL burden control. ARIMA projections suggested declining mortality and DALYs but heterogeneous future trends in incidence and prevalence by sex. Conclusions: Despite improvements in age-standardized mortality and DALYs, the overall burden of AF/AFL in China continues to increase, primarily driven by population aging. Targeted prevention, early detection, and optimized management strategies - particularly among older adults and high-risk males - are urgently needed.
Heart Failure (HF) represents the terminal stage of various cardiac diseases and is classified into Acute Heart Failure (AHF) and Chronic Heart Failure (CHF) based on the onset speed. Both are characterized by impaired myocardial function, neurohumoral disturbance, and ventricular remodeling, yet exhibit significant differences in pathophysiological mechanisms and clinical phenotypes. MicroRNAs (miRNAs), a class of non-coding RNAs approximately 18-25 nucleotides in length, regulate gene expression at the post-transcriptional level by targeting the 3' untranslated region (3'UTR) of target gene messenger RNAs. They are extensively involved in physiological and pathological processes such as cell proliferation, apoptosis, and fibrosis. A growing body of evidence has confirmed that abnormal miRNA expression profiles are closely associated with the occurrence and progression of HF, playing a crucial regulatory role in the pathological processes of both AHF and CHF. This review systematically examines the biological characteristics of miRNAs and elaborates on their core regulatory roles in the pathophysiological mechanisms of AHF and CHF. It analyzes differences and commonalities in miRNA expression and function between the two conditions, and explores the clinical application prospects of miRNAs as diagnostic markers, prognostic indicators, and therapeutic targets for HF. Finally, it summarizes current research challenges and future directions, aiming to provide a theoretical basis for the precise diagnosis and treatment of HF.
Aim: To identify factors associated with late atrial fibrillation (AF) recurrence after radiofrequency catheter ablation and to develop a nomogram for individualized risk prediction, followed by external validation in an independent cohort. Methods: We conducted a retrospective cohort study of patients with AF who underwent catheter ablation at Tongji Hospital (training cohort, January 2020-December 2022) and the Second Hospital of Lanzhou University (validation cohort, June 2020-June 2023). Follow-up visits were scheduled at 1, 3, 6, 12, and 18 months after the procedure. Candidate predictors were identified using the Boruta algorithm and the least absolute shrinkage and selection operator. Selected variables were then entered into multivariable Cox proportional hazards models. Model performance was evaluated using Harrell’s C-index, time-dependent area under the receiver operating characteristic curve, calibration plots, and decision curve analysis. Results: A total of 256 patients in the training cohort and 203 in the validation cohort were included, with a median follow-up of 12 months. Late AF recurrence occurred in 21.9% and 21.2% of patients, respectively. Six variables were included in the final model: early recurrence (HR = 7.616), left atrial diameter (HR = 1.684), intraoperative electrical cardioversion (HR = 1.423), serum creatinine (HR = 1.018), use of angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB)/angiotensin receptor-neprilysin inhibitor (ARNI) (HR = 0.426), and AF duration (HR = 1.003). The nomogram showed good discrimination, calibration, and clinical usefulness in both cohorts. Conclusion: We developed and externally validated a six-variable nomogram for predicting late AF recurrence after catheter ablation. This model may support individualized risk stratification and guide post-ablation management.
Heart failure (HF), a major cause of cardiovascular mortality worldwide, develops through a multifaceted process involving cardiomyocyte apoptosis and necrosis, metabolic dysregulation, fibrosis, and sustained inflammatory activation. Although B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) are routinely used in clinical assessment, their susceptibility to external influences limits their capacity to fully capture the molecular progression of HF. Emerging evidence has identified long non-coding RNAs (lncRNAs) as important epigenetic regulators that contribute to reduced myocardial contractility and ventricular remodeling. Clinical studies further indicate that circulating lncRNAs - particularly those packaged within exosomes - possess notable stability and strong disease specificity, making them promising candidates for improving diagnostic and prognostic evaluation. With ongoing advances in transcriptomic profiling and exosome-based technologies, the potential use of lncRNAs is also extending into forensic identification. This review synthesizes current insights into lncRNA-mediated regulation in HF progression, evaluates recent developments in circulating lncRNA detection, and explores their emerging forensic applications. It also outlines key limitations in existing research and discusses future directions to support deeper investigation into the molecular mechanisms underlying cardiac death and their relevance to forensic practice.
Small nucleolar RNAs (snoRNAs) are increasingly recognized as key regulatory factors in cardiovascular disease (CVD), with functions that extend far beyond the traditional scope of ribosomal RNA modification. This review synthesizes current knowledge regarding the biology of snoRNAs and their emerging roles in CVD, aiming to provide a clear theoretical framework for their pathogenic mechanisms and clinical significance. We first discuss the biogenesis, classification, and functional diversity of snoRNAs, covering both classical modification roles and non-classical functions such as the regulation of messenger RNA splicing, participation in the DNA damage response, and the generation of snoRNA-derived small RNAs. In CVD, snoRNAs exhibit spatiotemporal dysregulation and are extensively involved in pathological processes ranging from congenital heart defects and cardiomyopathy to coronary artery disease, myocardial infarction, arrhythmias, and heart failure. Specific gene clusters, particularly 14q32 snoRNAs, repeatedly emerge as key regulatory nodes in processes such as vascular remodeling and platelet activation. However, the majority of dysregulated snoRNAs remain orphaned with unknown targets, limiting our understanding of their mechanisms and clinical translation. We emphasize that combining computational modeling with multi-omics approaches can accelerate target identification and functional elucidation. Finally, we systematically examine the opportunities and challenges facing the clinical translation of snoRNA research, including their potential as dynamic biomarkers, limitations of detection technologies, and barriers to therapeutic delivery. By comprehensively reviewing existing evidence and future directions, this review highlights the significant potential of snoRNAs as novel biomarkers and therapeutic targets for the precision diagnosis and treatment of cardiovascular diseases.
Aim: Maternal overnutrition predisposes offspring to an increased prevalence of cardiovascular disease, yet the specific underlying mechanisms remain elusive. Methods: This study examined the roles of inflammation and ferroptosis in driving fetal cardiac structural and functional alterations following maternal overnutrition. Multiparous ewes were fed either a control diet [100% of National Research Council (NRC) recommended requirements] or an overnutrition diet (150% of NRC requirement) from 60 days preconception until gestational day 135. Cardiac geometry, histomorphology, immune cell infiltration, cardiomyocyte function, intracellular Ca2+ handling, and expression of inflammatory and ferroptotic markers were assessed in fetal hearts. Results: Despite comparable fetal crown-rump lengths and organ weights (e.g., brain and liver), fetuses from overnourished ewes exhibited significantly lower body and heart weights. Maternal overnutrition induced marked cardiac atrophy, interstitial fibrosis, lipid deposition, and oxidative damage, coupled with increased neutrophil and monocyte infiltration. At the cellular level, cardiomyocytes from overnourished fetuses exhibited impaired contractile and intracellular Ca2+ properties. Molecular profiling revealed that maternal overnutrition significantly upregulated proinflammatory markers (CD14, CD68, IL1A, IL1B, IL6, TLR4, and iNOS), and increased IκB phosphorylation (indicating NFκB activation). Concurrently, overnutrition suppressed IL18 and M-CSF expression, alongside the ferroptosis-defense proteins GPX4 and SLC7A11. Conclusion: These findings demonstrate that maternal overnutrition creates a proinflammatory and ferroptosis-prone myocardial environment, resulting in pathological structural remodeling and functional impairment of fetal hearts. Our data suggest that targeting the inflammation-ferroptosis signaling may help to mitigate the developmental programming of cardiovascular disease.
Aim: We aimed to resolve the paradoxical associations of limb circumference—inverse with mortality but positive with cardiovascular risk factors (CVRFs)—by systematically comparing the predictive value of the ratio of combined arm and thigh circumference (ATC) to waist circumference (WC) against that of the sum of ATC for mortality and key CVRFs. Methods: Our analysis utilized data from 17,276 U.S. participants in the 1999-2006 NHANES (National Health and Nutrition Examination Survey). We utilized Cox proportional hazards, generalized linear, and restricted cubic spline models, with comprehensive adjustment for confounders including adiposity. The outcomes assessed were all-cause and cardiovascular mortality, hypertension, diabetes, and resting tachycardia. Results: During median 18.04-year follow-up (3,927 deaths, 1,047 cardiovascular deaths), the highest versus lowest ATC/WC quartile showed consistently protective associations: all-cause mortality (hazard ratio (HR) = 0.47, 95% confidence interval (95%CI): 0.38-0.57), cardiovascular mortality (HR = 0.32, 0.21-0.49), hypertension (OR = 0.49, 0.41-0.59), diabetes (odds ratio (OR) = 0.26, 0.18-0.37), and resting tachycardia (OR = 0.28, 0.19-0.39; all P < 0.001). Conversely, ATC exhibited adiposity-dependent paradoxical associations: protective for mortality but harmful for CVRFs when unadjusted for adiposity. After adiposity adjustment, ATC's harmful CVRFs associations were attenuated or reversed, while mortality benefits persisted. ATC/WC demonstrated superior linearity in dose-response relationships compared to ATC. Conclusion: The ATC/WC ratio consistently demonstrates protective associations with both mortality and CVRFs. The waist standardization approach clarifies the relationship between limb measurements, cardiovascular health, and mortality by adjusting for central adiposity-related confounding that limits the utility of absolute rather than relative peripheral limb measurements.
Atherosclerosis research has been significantly advanced by mouse models, particularly genetically engineered strains such as apolipoprotein E-deficient mice and low-density lipoprotein receptor-deficient mice (Ldlr-/-). These mouse models replicate the hyperlipidemia-driven plaque pathogenesis, providing critical insights into lipid metabolism, inflammation, and therapeutic responses. Classic models play an important role in validating the effects of lipid-lowering therapies such as statins and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. There are also some limitations, including species-specific lipoprotein profiles and incomplete replication of advanced human plaque complexity. Novel models have emerged to address these gaps, incorporating features such as hemodynamic stress, humanized lipid metabolism, and inducible gene regulation to complement the inadequacies of classic models, thereby better simulating the multifactorial complexity of atherosclerosis. For example, adeno-associated virus serotype 8 carrying the Pcsk9[D377Y] mutant gene and Ldlr-antisense oligonucleotide mice integrate hemodynamic stress, humanized lipid metabolism, and multifactorial comorbidities. However, there are still some shortcomings, including metabolic disparities, inadequate modeling of plaque rupture/thrombosis, and oversimplification of systemic disease interactions. Future directions prioritize next-generation models featuring humanized lipoprotein profiles, dynamic gene regulation, and combined with metabolic syndrome features. These approaches can be synergized with advanced phenotyping tools—including single-cell omics and intravital imaging—alongside artificial intelligence-driven multi-omics integration. By bridging translational gaps between murine pathophysiology and human disease complexity, these mouse models promise to accelerate the development of atherosclerosis therapies.
Heart failure (HF) is a syndrome of global concern with high morbidity and mortality, whose complex molecular regulatory mechanisms are not yet fully understood. Moving beyond the traditional research framework focused on microRNAs, long non-coding RNAs (ncRNAs), and circular RNAs, this review concentrates on the pivotal roles of emerging ncRNAs - specifically Piwi-interacting RNAs (piRNAs), transfer RNA-derived small RNAs (tsRNAs), and small nucleolar RNAs (snoRNAs) - in the pathological progression of HF. In the acute phase of HF, these molecules rapidly respond to stressors such as ischemia and hypoxia. They directly influence cardiomyocyte fate and acute injury outcomes by regulating processes including apoptosis, necroptosis, autophagy, and inflammatory responses. During the chronic phase, they are deeply involved in pathological myocardial remodeling. They precisely regulate cardiomyocyte hypertrophy, cardiac fibroblast activation, and interstitial fibrosis in a cell-specific manner, maintaining a fine-tuned balance between pro-pathological and protective functions. These discoveries significantly enrich the molecular regulatory map of HF and reveal the considerable potential of these ncRNAs as novel non-invasive biomarkers and promising therapeutic targets. Of particular note, strategies employing engineered exosomes to deliver specific snoRNAs have demonstrated therapeutic effects in preclinical models, such as reversing fibrosis and improving cardiac function. This marks a shift in the treatment paradigm for HF toward precise RNA-level regulation.
Aim: To evaluate the long-term impact of obstructive sleep apnea (OSA) risk profile on atrial fibrillation (AF) recurrence after catheter ablation in patients with paroxysmal AF. Methods: This prospective study enrolled 161 patients with paroxysmal AF undergoing initial ablation. Patients were stratified by the Berlin Questionnaire (BQ) into high-risk (n = 94) and low-risk (n = 67) OSA groups. Atrial tachyarrhythmias occurring within the initial three months were defined as early recurrence, whereas recurrence beyond three months was defined as late recurrence. A subgroup of 71 patients with recurrence underwent a redo ablation. Results: After 16.1 ± 0.4 years, multivariable models revealed that a BQ-defined high OSA risk was independently associated with early recurrence (odds ratio [OR] 1.99, 95% confidence interval [CI] 1.02-3.86, P = 0.043), whereas it was not independently associated with late recurrence after the initial procedure (hazard ratio [HR] 1.05, 95%CI: 0.70-1.57, P = 0.810). Cox regression identified early recurrence (HR 2.95, 95%CI: 1.99-4.39, P < 0.001) and baseline high-sensitivity C-reactive protein (hs-CRP; HR 1.02, 95%CI: 1.00-1.03, P = 0.022) as independent predictors of late recurrence after the initial procedure. Following redo ablation, early recurrence remained a strong independent predictor (HR 5.93, 95%CI: 2.13-16.50, P < 0.001). Conclusions: The BQ-defined high OSA risk was an independent predictor of early recurrence; however, it was not significantly associated with late recurrence after AF ablation. Early recurrence was the strongest predictor of long-term outcome, highlighting the importance of management during the post-procedural blanking period.
Cardiovascular diseases (CVDs) involve structural and functional abnormalities of the heart and blood vessels, in which genetic factor plays a significant role. Non-coding RNAs (ncRNAs), as important products of genetic material, are important contributors to CVDs. They mainly regulate the expression of targets and participate in various biological processes such as cell proliferation, cell apoptosis, and signal transduction. Genetic variation in ncRNAs can affect the expression levels of ncRNAs themselves and their downstream targets, leading to the dysregulation of biological processes and contributing to the occurrence and development of CVDs. This review aims to summarize the current research status of ncRNA genetic variation in CVDs and clarify the functions and biological mechanisms of ncRNA genetic variation involved in CVDs.
Heart failure (HF) is a complex syndrome driven by structural remodeling, fibrosis, metabolic imbalance, and oxidative stress. Circular RNAs (circRNAs) have emerged as pivotal regulators in HF, distinguished by their covalently closed structure, stability, and tissue specificity. While they modulate myocardial hypertrophy, fibrosis, and metabolic pathways through mechanisms including microRNA (miRNA) sponging, protein interactions, and transcriptional regulation, emerging evidence highlights their critical role in regulating intracellular Ca2+ homeostasis and excitation-contraction (E-C) coupling. By modulating key calcium-handling proteins, circRNAs directly influence cardiomyocyte contractility and arrhythmia susceptibility, linking RNA networks to dynamic cardiac function beyond structural remodeling. Beyond their mechanistic roles, the inherent stability and tissue-specificity of circRNAs position them as highly promising biomarkers for early diagnosis, risk stratification, and therapeutic monitoring. Furthermore, their therapeutic potential is rapidly unfolding; strategies involving extracellular vesicle delivery or targeted silencing offer viable cell-free approaches to inhibit fibrosis and restore cardiac function. This review systematically dissects the multifaceted roles of circRNAs in HF, from their fundamental impact on pathophysiology to their translational journey as biomarkers and therapeutic targets. We also explore current challenges and future directions, providing a comprehensive theoretical framework for the development of circRNA-based precision interventions for heart failure.
The integrity of the vascular endothelium is fundamental to its barrier function, maintaining vascular homeostasis and microenvironmental stability, and serves as a prerequisite for preventing certain vascular diseases. After vascular integrity is compromised, endothelial progenitor cells (EPCs), a diverse population of progenitor cells with the capacity to develop into endothelial cells, can reconstruct blood vessels. This occurs primarily through two mechanisms: (1) direct integration into existing vessels for repair; and (2) paracrine secretion of proangiogenic factors to promote EPC mobilization and migration, regulate immune functions, and inhibit endothelial hyperplasia. This review aims to elucidate the mechanisms by which EPCs participate in vascular remodeling, and to discuss the latest advances in clinical translation strategies such as cell therapy, EPC-derived exosome therapy, and EPC functional modulation, as well as the current challenges in standardization and clinical application.
Heart failure (HF) is characterized by profound mitochondrial dysfunction, a central pathogenic mechanism driven by interconnected defects in metabolic dysregulation, excessive oxidative stress, impaired biogenesis, imbalanced dynamics, and defective mitophagy. This compromised mitochondrial fitness leads to bioenergetic deficiency, cardiomyocyte death, and progressive cardiac remodeling. MicroRNAs (miRNAs) have emerged as critical post-transcriptional regulators of mitochondrial homeostasis, capable of simultaneously modulating multiple components within these pathways. By fine-tuning the expression of key genes involved in fission/fusion, mitophagy, and biogenesis, miRNAs can either exacerbate or ameliorate HF progression, forming a complex and context-dependent regulatory network, and highlighting the potential of targeting the miRNA-mitochondria axis. However, clinical translation faces significant hurdles including target specificity, tissue-selective delivery and patient heterogeneity. Future research should focus on deciphering the mechanistic interplay between miRNA regulation and mitochondrial function in diverse HF contexts. This review aims to elucidate the molecular mechanisms by which miRNAs regulate mitochondrial dysfunction in HF, revealing novel therapeutic targets. A deeper understanding of this regulatory network is crucial for advancing HF management from symptom palliation toward mechanism-based precision medicine.
Cardiovascular diseases (CVDs) are among the leading causes of global morbidity and mortality, placing a substantial burden on public health and socioeconomic development. Early and accurate diagnosis is essential for reducing CVDs mortality and optimizing individualized treatment strategies. Although conventional detection methods, such as enzymatic analysis and immunoassays, have reached a relative level of maturity in clinical applications, they are still constrained by high costs, complex procedures, and limited real-time capabilities. In recent years, electrochemical immunosensors have shown significant potential for detecting CVD-related biomarkers, owing to their advantages of high sensitivity, excellent selectivity, rapid response, and portability. In this review, we explore the latest advancements in electrochemical immunosensors for CVDs research, analyze innovative designs and fabrication techniques for various sensor types, and summarize their applications in detecting CVD-related biomarkers.
Ischemia-reperfusion injury (IRI) is a pathophysiological process occurring after blood supply restoration to tissues or organs, causing unexpected cellular damage. It involves multiple complex mechanisms, but inflammation and oxidative stress are the main causes. IRI can damage vital organs such as the heart, brain, liver, and kidneys, affecting patient prognosis and quality of life. Therefore, the prevention and treatment of IRI have become a key area in clinical and basic research. Prussian blue, a metal-organic framework material, is approved by the U.S. Food and Drug Administration for treating heavy metal poisoning. In 2016, research indicated that Prussian blue nanoparticles had multi-enzyme activities like catalase, peroxidase, and superoxide dismutase, enabling them to scavenge reactive oxygen species and combat inflammation, establishing them as a highly promising nanozyme. Leveraging their unique antioxidative and anti-inflammatory properties, Prussian blue nanozyme (PBNZ) can directly target key pathological pathways of IRI. Furthermore, PBNZ can serve as efficient drug delivery systems, and through functional modifications, they enable the targeted delivery of therapeutic agents, thereby synergistically enhancing treatment efficacy. Currently, PBNZ have demonstrated significant therapeutic potential in IRI models involving various organs and tissues such as the heart, brain, liver, kidneys, and skin flaps. This review aims to outline IRI's key pathological mechanisms, analyze how PBNZ combats oxidative stress and inflammation, and summarize its recent application advancements in treating IRI in different organs. The goal is to offer theoretical reference and research insights for the future development of novel nanozyme-based therapeutic strategies against IRI.
Intracardiac echocardiography (ICE) has become an indispensable real-time imaging modality in atrial fibrillation (AF) ablation procedures, offering distinct advantages across multiple domains, including pre-procedural exclusion of left atrial appendage (LAA) thrombus, real-time guidance for transseptal puncture, catheter localization during ablation, anatomical assessment for LAA closure, and monitoring of complications such as pericardial effusion. Recent investigations have further expanded its utility, particularly in pre-ablation LAA thrombus screening and in guiding emerging pulsed-field ablation techniques. Beyond procedural navigation, ICE enables early detection and timely management of potentially serious complications, while also substantially reducing radiation exposure during transseptal puncture. This review provides a comprehensive overview of the broadening applications of ICE in AF catheter ablation and related interventions, with a specific focus on its current roles in AF ablation and LAA occlusion. The synthesized evidence offers a valuable framework for optimizing future clinical strategies that integrate ICE into AF diagnosis and treatment. Given its considerable benefits in enhancing both safety and efficacy, the broader adoption of ICE in these procedures is strongly warranted.
