Immune checkpoint inhibitor (ICI)-related myocarditis is a rare but often fatal adverse event that has gained increasing attention due to the widespread clinical use of ICIs. This review explores the development of immune cells and their critical roles in cardiac autoimmunity, with particular focus on defects in central tolerance, the role of immune checkpoints, T cell trafficking to the heart, and the involvement of resident cardiac macrophages. It also introduces the key pathogenic mechanisms of ICI-related myocarditis, including the activation of autoreactive T cells that recognize self or shared antigens, the crosstalk between T cells and macrophages, and macrophage polarization. In addition, we also discuss current and emerging targetable therapeutic pathways, including cytokine modulation, the JAK/STAT pathway, and the use of CTLA-4 immunoglobulin. We further summarize practical diagnostic and prognostic approaches, including the role and limitations of troponin-based monitoring, echocardiography, magnetic resonance imaging, PET-CT applications, and endomyocardial biopsy. This review aims to establish a mechanistic framework that integrates pathogenic mechanisms, diagnostic and prognostic approaches, and therapeutically targetable pathways in ICI-related myocarditis.

Ischemic stroke disproportionately impacts the elderly with a higher risk and poor repair. Current therapeutic options are constrained by narrow time windows, strict contraindications, and suboptimal efficacy in older patients, leaving a critical unmet clinical need. Hypoxia-based interventions exert preclinical neuroprotective effects, yet the effects and underlying mechanisms of intermittent hypoxia (IH) in elderly patients with ischemic stroke remain unclear.

This study tested IH in 25-month-old C57BL/6J mice with photothrombotic (PT) stroke, randomizing to Control, PT, or PT+IH groups. IH post-conditioning was administered a total of 7 sessions on days 3-16. One session consists of a 10-min phase with 8% oxygen, followed by a 10-min phase with room air. Behavioral changes were measured through the maximal grip strength test, beam balance test, cylinder test, adhesive removal test, grid-walking test, and open field test. Neuropathological changes and potential molecular mechanisms were analyzed via immunofluorescence staining and western blotting.

Our findings demonstrated that IH treatment significantly reduced cortical infarct volume and ameliorated PT-induced sensorimotor deficits in aged mice. Furthermore, IH alleviated neuronal damage and apoptosis, preserved cerebrovascular morphology, and attenuated excessive astrocyte-vasculature interactions. Mechanistically, IH upregulated astrocyte-specific hypoxia-inducible factor 1α (HIF-1α), mitigated mitochondrial fragmentation, and shifted the polarization of microglia and astrocytes from pro-inflammatory (M1/A1) to anti-inflammatory (M2/A2) phenotypes. Collectively, these effects contributed to enhanced neurogenesis and angiogenesis in the peri-infarct region.

In conclusion, these findings confirm IH's neurorestoration in aged stroke mice, potentially via HIF-1α-related regulation of mitochondrial function, glial polarization, and vascular integrity, supporting its translational potential.

Myocardial ischemia-reperfusion injury (MIRI) induces oxidative stress and inflammatory signaling that drive fibroblast activation, myocardial fibrosis, and progressive cardiac dysfunction, for which effective targeted therapies remain limited. The electrophilic fatty acid nitroalkene 10-nitro-octadec-9-enoic acid (NO₂-FA) exhibits anti-inflammatory and antifibrotic properties but pharmacological actions have been limited by extents of myocardial delivery. Ultrasound-targeted cavitation (UTC) using lipid-shelled gas-filled nanoparticles (LNPs) enables spatially controlled drug release and represents a promising theranostic strategy.

NO₂-FA were incorporated in LNPs and delivered focally to the myocardium using UTC. Therapeutic efficacy was evaluated in rodent models of MIRI and myocardial fibrosis. In the MIRI model, animals received UTC + NO₂-FA LNPs, intravenous NO₂-FA, or sham treatment. Cardiac structure, function, and molecular remodeling were assessed using echocardiography, histological staining, polymerase chain reaction, and enzyme-linked immunosorbent assay. In the myocardial fibrosis model, additional analyses included immunohistochemistry and cardiovascular magnetic resonance imaging.

UTC-mediated delivery of NO₂-FA LNPs significantly reduced myocardial fibrosis compared with intravenous NO₂-FA (p = 0.03) and sham treatment (p = 0.001), as demonstrated by histological quantification and reduced late gadolinium enhancement. Targeted NO₂-FA delivery also improved cardiac output and favorably modulated molecular markers associated with fibrosis and inflammation. Across both experimental models, UTC-facilitated NO₂-FA delivery consistently demonstrated superior therapeutic efficacy relative to non-targeted administration.

Spatially targeted delivery of NO₂-FA using ultrasound-mediated cavitation enhances cardioprotective and antifibrotic effects in experimental models of MIRI and myocardial fibrosis. This platform integrates targeted therapy with imaging-based assessment and supports further development of UTC-enabled theranostic approaches for ischemic heart disease.

Mitochondrial bioenergetic competence critically depends on cristae architecture, which is organized and stabilized by the mitochondrial contact site and cristae organizing system (MICOS) complex. As a core MICOS subunit, CHCHD3 (also known as MIC19) contributes to assembly of the mitochondrial intermembrane space bridging (MIB) supercomplex and regulates cristae morphology, endoplasmic reticulum-mitochondria contact sites, and cellular metabolic homeostasis. Aberrant CHCHD3 expression or functional deficiency is implicated in the pathogenesis of neurodegenerative disorders, cardiovascular diseases, metabolic syndromes, and cancers. Notably, CHCHD3 function is governed by a dose-dependent "Goldilocks" principle, wherein both insufficient and excessive expression-as well as preserved abundance with impaired functional integrity-can compromise mitochondrial homeostasis, underscoring the need for context-specific therapeutic modulation. Here, we systematically summarize CHCHD3 molecular characteristics and post-translational modification networks, with emphasis on its roles in energy metabolism, organelle crosstalk, and apoptosis. We further examine the mechanistic links between CHCHD3 dysregulation and disease pathogenesis, evaluate current targeting strategies and their pharmacological limitations, and identify remaining controversies and knowledge gaps to guide future research toward clinical translation.

Cardiovascular diseases are the leading cause of death worldwide, and accurate assessment of left ventricular volume (LVV) is crucial for diagnosis, therapy guidance, and long-term monitoring in these patients. Existing clinical techniques either require substantial resources, depend strongly on operator expertise, or lack the precision required for continuous monitoring. In this work we investigate the feasibility of a finite-element- method-based (FEM) algorithm for estimating volume and catheter offset from catheter-based admittance measurements to provide the basis for a new LVV estimation method. The present paper describes the underlying ventricle FEM model, a sensitivity-guided selection of informative 4-electrode configurations, and a constrained Gauss-Newton estimation algorithm. The algorithm was evaluated using numerical simulations and measurements obtained with a dynamic 3D-printed ventricle phantom with controllable volume changes. In both simulation and experiment, the reduced measurement set achieved volume reconstructions comparable to the full measurement set. In the phantom experiments, volume estimation errors of approximately 3-4% were observed over a wide range of volumes. These results demonstrate the feasibility of FEM-based parameter estimation and show that a small number of optimized electrode configurations can provide sufficient information for robust volume estimation. While the present study uses simplified geometries and a controlled phantom setup, the proposed approach provides a methodological basis for future investigations using more realistic anatomical models and biological experiments.

Hypertension, a leading modifiable risk factor for cardiovascular diseases, is projected to contribute substantially to the global burden of cardiovascular health by 2050. Sleep has emerged as a potential factor in the prevention and management of hypertension. This review synthesizes recent evidence on the relationship between sleep health dimensions and hypertension, highlighting clinical significance, identifying gaps, and outlining future research directions.

Prolonged sleep latency, greater wake after sleep onset, both short and long sleep duration, poor overall sleep quality, and reduced sleep efficiency are associated with a higher risk of hypertension. However, most studies are cross-sectional and rely primarily on subjective measures, often limited to sleep duration.

A multidimensional approach to sleep health may reduce hypertension risk and improve blood pressure control. More longitudinal and intervention studies in varied populations are needed to develop tailored sleep health recommendations and guide clinical guidelines.

The salivary microbiome plays a crucial role in both oral health and systemic diseases, offering significant insights into disease development and early diagnosis. Under normal conditions, a balanced relationship exists between the microbiota and the host; however, when this balance is disrupted, it can lead to the onset of oral diseases such as dental caries, periodontal disease, and oral cancer. Changes in the salivary microbiome provide valuable information for the early diagnosis of oral diseases. Moreover, microbial dysbiosis in the oral cavity may promote the translocation of pathogenic microorganisms via the gastrointestinal tract, lungs, or bacteremia, leading to ectopic colonization outside the oral cavity and contributing to the onset and progression of systemic diseases such as colorectal cancer, cardiovascular diseases, and autoimmune disorders. Therefore, this review summarizes the role of the salivary microbiome in disease development and diagnosis, based on recent advancements in research on salivary microbiota, offering new perspectives for the early prevention and clinical management of systemic diseases.

To systematically identify traditional Chinese medicine (TCM) compound formulas with anti-atherosclerosis (AS) potential using a screening platform based on multi-strain apoeb gene knockout zebrafish models for anti-atherosclerosis TCM compounds.

Screening was conducted using a formula dictionary database, and compound formulas such as Dan Shen Fang, Shang Ni San, Jin Lingzi San, and Li Qi Hua Liang Tang were selected from 933 blood-activating and stasis-resolving formulas. Five strains of apoeb ^－/－ zebrafish-AB, Tg(mpeg1:EGFP), Tg(lyzc:dsRed), Tg(gata1a:mCherry), and Tg(flk1:EGFP)-were fed a high-fat diet for 2 days, after which the AS model was established. DMSO (solvent control), rosuvastatin (western medicine positive control), compound Dan Shen Fang (TCM positive control), Shang Ni San, Jin Lingzi San, and Li Qi Hua Liang Tang were administered by bathing for 24 hours. Oil red O staining was used to detect lipid content, oxidative stress indicators, blood flow velocity, vascular endothelial cell damage, and the expression of inflammatory factors in zebrafish. The behavior patterns of inflammatory cells in zebrafish were observed, and the anti-AS efficacy of the Li Qi Hua Liang formulas was comprehensively evaluated.

Compared with the AS model group, compound Dan Shen Fang and Shang Ni San improved lipid accumulation in the vascular lumen, reduced total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) levels, decreased oxidative stress response, inhibited the recruitment of neutrophils and macrophages, repaired vascular endothelial damage, improved blood flow velocity, and reduced the expression of inflammatory factors, thereby alleviating AS, with statistically significant differences. Jin Lingzi San and Li Qi Hua Liang Tang had limited effects on AS.

This platform provides an efficient and targeted tool for the screening and research evaluation of anti-atherosclerosis TCM compound formulas, accelerates the research progress of anti-atherosclerosis TCM compound formulas, and lays a foundation for subsequent drug development and clinical application.

The renin-angiotensin system (RAS) plays a central role in regulating blood pressure and cardiovascular health. Angiotensin-converting enzyme (ACE) facilitates the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor that contributes to hypertension and heart failure. Conversely, ACE2 converts angiotensin II into angiotensin-(1-7), a vasodilator with protective cardiovascular effects. An imbalance between ACE and ACE2 activities has been increasingly associated with the progression of cardiovascular diseases and complications related to COVID-19. This review analyzed 100 relevant studies published up to May 2024, identified through a comprehensive literature search on PubMed and Scopus. The findings highlighted that dysregulation of the ACE/ACE2 axis exacerbates cardiovascular dysfunction. The interaction of SARS-CoV-2 with ACE2 reduces its protective function, intensifying inflammatory responses and leading to complications such as lung injury and heart failure. Additionally, genetic polymorphisms in ACE and ACE2 influence individual susceptibility and severity of COVID-19. Promising therapeutic strategies, including ACE2-based peptides and angiotensin II receptor modulators, are under investigation but require further clinical validation. Targeting the ACE/ACE2 axis could provide effective treatment options for cardiovascular disease and COVID-19-related complications, warranting further in-depth research.

Cardiovascular diseases (CVDs) severely threaten human health, and microtubule dysfunction is one of the major contributing factors. Tubulin post-translational modifications (PTMs), such as detyrosination, acetylation, and polyglutamylation, regulate microtubule homeostasis, among which the upregulation of detyrosination is a key feature of cardiovascular diseases. Traditional Chinese Medicine (TCM) can alleviate cardiac pathologies by targeting these modifications. This review discusses the driving mechanisms of PTMs in relation to the pathological changes that occur in CVDs and summarizes the therapeutic effects of traditional Chinese Medicine targeting these modifications that have been identified in recent years. By systematically searching databases such as PubMed, it was found that PTMs primarily control the stability and contractility of the microtubule cytoskeleton in cardiomyocytes. Their dysregulation promotes the progression of diseases such as myocardial infarction (MI), atherosclerosis (AS), arrhythmias, and cardiac hypertrophy by disrupting key processes including mitochondrial energy metabolism, inflammasome activation, calcium homeostasis, and oxidative stress (OS). Certain active compounds found in TCM, such as curdione, evodiamine, and tanshinone IIA (Tan-IIA), can modulate PTMs through the synergistic regulation of multiple pathways. This review provides a theoretical basis for establishing TCM-based therapeutic strategies for CVDs that target PTMs.