Inflammatory bowel disease (IBD), encompassing Crohn's disease and ulcerative colitis, is increasingly recognized as a systemic condition with cardiovascular implications. Among these, heart failure has emerged as a significant complication. The aim of this narrative review was to explore the cellular and molecular pathways that link IBD and heart failure. Drawing upon findings from epidemiologic studies, experimental models, and clinical research, we examined the pathways through which IBD may promote cardiac dysfunction. Chronic systemic inflammation in IBD, driven by cytokines such as TNF-α and IL-1β, can impair myocardial structure and function. Furthermore, intestinal barrier dysfunction and gut dysbiosis can facilitate the translocation of proinflammatory microbial metabolites, including lipopolysaccharide and phenylacetylglutamine, and deplete cardioprotective metabolites like short-chain fatty acids, thereby exacerbating heart failure risk. Additional contributing factors include endothelial and microvascular dysfunction, autonomic dysregulation, nutritional deficiencies, shared genetic susceptibility, and adverse pharmacologic effects. IBD contributes to heart failure pathogenesis through multifactorial and interrelated mechanisms. Recognizing the role of the gut-heart axis in IBD is crucial for the early identification of cardiovascular risk, providing guidance for integrating care and developing targeted therapies to reduce the risk of heart failure in this vulnerable population.

Heart failure (HF), a prevalent global health issue characterized by the heart's impaired ability to pump or fill blood, affects millions worldwide and continues to pose significant challenges despite advancements in treatment. This review delves into the critical and increasingly recognized role of inflammation in the development and progression of this complex syndrome. While the incidence of HF has seen a decline in some regions due to improved cardiac care, its overall prevalence is rising, particularly among younger adults and those with heart failure with a preserved ejection fraction (HFpEF). Given the persistently high rates of hospitalization and mortality associated with HF, understanding the underlying mechanisms, including the contribution of inflammation, is crucial for identifying novel therapeutic strategies. Inflammation in heart failure is a multifaceted process involving the activation of the immune system, both innate and adaptive, and encompasses various mechanisms such as the release of pro-inflammatory mediators, endothelial dysfunction, and neurohormonal activation. Myocardial damage triggers the innate immune response, while humoral immunity and chronic systemic inflammation, often linked to cardiovascular risk factors and autoimmune diseases, also play significant roles. Notably, heart failure and inflammation have a reciprocal relationship, with HF itself contributing to inflammatory processes within the cardiac tissue and systemically. Understanding these intricate pathways, including the involvement of specific immune cells and molecular mediators, is essential for comprehending the pathogenesis of heart failure and exploring potential therapeutic interventions. The review further examines various inflammatory biomarkers that have been implicated in heart failure, such as cytokines (including TNF-α and IL-1) and C-reactive protein (CRP). While these markers often correlate with the severity and prognosis of HF, clinical trials targeting specific inflammatory mediators have largely yielded disappointing results, highlighting the complexity of the inflammatory response in this context. The exploration of these biomarkers and the challenges encountered in translating anti-inflammatory strategies into effective treatments underscore the need for continued research to unravel the precise role of inflammation across different HF subtypes and to develop more targeted and effective anti-inflammatory therapies.

Calcium channel blockers (CCBs), originally developed for cardiovascular indications, have gained attention for their therapeutic potential in neuropsychiatric, endocrine, and pain-related disorders. In neuropsychiatry, nimodipine and isradipine, both L-type CCBs, show mood-stabilizing and neuroprotective effects, with possible benefits in depression, bipolar disorder, and schizophrenia. In endocrinology, verapamil, a non-dihydropyridine L-type blocker, has been associated with the preservation of pancreatic β-cell function and reduced insulin dependence in diabetes. CCBs may also aid in managing primary aldosteronism and pheochromocytoma, particularly in patients with calcium signaling mutations. In pain medicine, α2δ ligands and selective blockers of N-type and T-type channels demonstrate efficacy in neuropathic and inflammatory pain. However, their broader use is limited by challenges in central nervous system (CNS) penetration, off-target effects, and heterogeneous trial outcomes. Future research should focus on pharmacogenetic stratification, novel delivery platforms, and combination strategies to optimize repurposing of CCBs across disciplines.

Heart-specific overexpression of transcriptional regulator JDP2 (jun dimerization protein 2) for 5 weeks provokes paroxysmal atrial fibrillation (AF) in mice. We now investigated whether AF and atrial remodeling will be reversible upon termination of JDP2 overexpression, and whether paroxysmal AF converts to permanent AF in the presence of maintained JDP2 overexpression. Cardiac-specific JDP2 overexpression for 5 weeks, resulting in paroxysmal AF, was either continued or repressed via a tet-off system for another 5 weeks. ECGs were recorded weekly. Thereafter, heart and lung weights, and atrial mRNA and protein expression were determined. Extending JDP2 overexpression did not aggravate the AF phenotype, still paroxysmal AF, prolongation of PQ intervals, and atrial hypertrophy were present. This phenotype was completely reversible upon cessation of JDP2 overexpression. A massive downregulation of connexin40 and calcium handling proteins, including SERCA2a, calsequestrin, and ryanodine receptor, was observed in atria after prolonged JDP2 overexpression. In conclusion, atrial remodeling and paroxysmal AF under JDP2 overexpression are not sufficient to maintain or aggravate AF in the absence of JDP2. The comparison of the two groups indicates that the downregulation of calcium proteins and connexins is an important factor in the maintenance of the disease.

The NADPH oxidase 2 (NOX2) complex is a critical regulator of immune homeostasis. It is utilized by phagocytic leukocytes including neutrophils, monocytes, and macrophages to generate reactive oxygen species (ROS) that drive microbe clearance and modulate inflammatory responses. Within NOX2, the essential scaffold protein p47phox plays a pivotal role in orchestrating enzyme activation and facilitating the assembly and membrane translocation of cytosolic components of the complex. Tight regulation of p47phox activity is crucial, and its disruption is linked to a number of pathological conditions. Conversely, its hyperactivity contributes to oxidative stress, tissue damage, the progression of cardiovascular diseases, neurodegenerative disorders, inflammatory conditions, metabolic syndromes, and cancer. In this review, we detail the structural and functional roles of p47phox, mechanisms of its regulation, and its multifaceted contributions to disease pathogenesis. We explore the latest advances in p47phox-targeted therapeutic strategies, discuss current challenges in the field, highlight p47phox's potential as a transformative target in redox biology and propose future directions to unlock its clinical utility.

Early identification of left ventricular ejection fraction (LVEF) levels during the progression of hypertension is essential to prevent cardiac deterioration. However, achieving a non-invasive, cost-effective, and definitive assessment is challenging. It has prompted us to develop a comprehensive machine learning framework for the automatic quantitative estimation of LVEF levels from electrocardiography (ECG) signals.

We enrolled 200 hypertensive patients from Zhongshan City, Guangdong Province, China, from 1 November 2022 to 1 January 2025. Participants underwent 24 h Holter monitoring and echocardiography for LVEF estimation. We developed a comprehensive machine learning framework that initiated with preprocessed ECG signal in one-hour intervals to extract CMSE-based heart rate variability (HRV) features, then utilized machine learning models such as linear regression (LR), Support Vector Machines (SVMs), and random forests (RFs) with recursive feature elimination for optimal LVEF estimation.

The LR model, notably during early night interval (20:00-21:00), achieved a RMSE of 4.61% and a MAE of 3.74%, highlighting its superiority. Compared with other similar studies, key CMSE parameters (Scales 1, 5, Slope 1-5, and Area 1-5) can effectively enhance regression models' estimation performance.

Our findings suggest that CMSE-derived circadian HRV features from Holter ECG could serve as a non-invasive, cost-effective, and interpretable solution for LVEF assessment in community settings. From a machine learning interpretable perspective, the proposed method emphasized CMSE's clinical potential in capturing autonomic dynamics and cardiac function fluctuations.

Arterial hypertension (HTN) is a growing global health concern, with limited tools available for early detection. Previous studies identified the overexpression of the epithelial sodium channel (ENaC) as a potential biomarker for HTN. In this work, we optimized and clinically validated a lateral flow immunoassay (LFIA) using gold nanoparticles (AuNPs) functionalized with anti-ENaC antibodies. The test strips were prepared with 10 µL of each component and performed in a 9-point herringbone format. For validation, a double-blind study was conducted using platelet lysates from 200 individuals, classified based on real-time blood pressure measurements. ENaC expression was assessed via both LFIA and Western blotting, which served as the reference method. Receiver operating characteristic (ROC) analysis yielded an AUC of 0.7314 for LFIA and 0.6491 for the Western blot, with LFIA demonstrating higher sensitivity (76.24%) and comparable specificity (61.54%) compared to the Western blot (68.31% and 60.34%, respectively). These results support LFIA as a practical, rapid, and moderately accurate tool for screening ENaC levels and identifying individuals at risk of hypertension.

Cardiovascular disease (CVD) is very widespread in countries with a Western-style diet, representing one of the major causes of morbidity. Genetic factors, obesity, diabetes, dyslipidemia, smoking, and ageing are risk factors for CVD outcomes. From a pathogenic point of view, the condition of low-grade inflammation of the arteries leads to endothelial damage and atherosclerosis development. Nowadays, a broad range of drugs is available to treat CVD, but many of them are associated with side effects. Therefore, alternative therapeutic remedies need to be discovered in combination with conventional drugs. A balanced diet rich in fruits and vegetables, e.g., the Mediterranean diet, has been shown to lower the incidence of CVD. Plant-derived polyphenols are ingested in food, and these compounds can exert beneficial effects on human health, such as antioxidant and anti-inflammatory activities.

In the present review, the cellular and molecular bases of the beneficial effects of polyphenols in the prevention and treatment of CVD will be pointed out.

This review has been conducted on the basis of a literature review spanning mainly the last two decades.

We found that an increased dietary intake of polyphenols is associated with a parallel decrease in chronic disease incidence, including CVD.

Despite a plethora of preclinical studies, more clinical trials are needed for a more appropriate treatment of CVD with polyphenols.

Cholangiocarcinoma, malignancies arising from the intrahepatic and extrahepatic bile ducts, has increased in incidence in the United States over the past few decades. The reported incidence of cholangiocarcinomas is high, particularly in specific racial groups such as Asian and Pacific Islander patients. Race also significantly impacts disparities in healthcare utilization and clinical outcomes. Our study focused on the impact of race on admission, clinical outcomes, and disposition of cholangiocarcinoma.

We performed a retrospective analysis of cholangiocarcinoma-related hospital admissions, using the National Inpatient Sample for the year 2022. Patients were stratified according to race into the following groups: White, African American, Hispanic, Asian or Pacific Islander, Native American, and Other. The data analysis was performed using STATA/BE version 18.5. Univariable and multivariable logistic regression models were applied to evaluate the relationship between race and clinical and healthcare utilization outcomes.

In 2022, 7479 hospitalizations were recorded for cholangiocarcinoma in the United States. Among these, 65.99% were White, 13.27% Hispanic, and 10.13% African American. There was a statistically significant difference in gender distribution across racial groups (p < 0.001), with males comprising the majority in all groups. Males outnumbered females in all racial groups except among the Hispanic group. Significant racial disparities in mortality were observed, with White patients showing a mortality rate of 6.69%, compared to higher rates among African American (9.76%), Native American (8.51%), and Asian or Pacific Islander (8.09%) patients, while Hispanic (5.04%) and Other (5.88%) groups had lower rates (p < 0.001).

The study underscores the racial disparities among cholangiocarcinoma hospitalizations, with African American, Native American, and Asian patients facing disproportionately higher mortality and poorer in-hospital outcomes compared to White patients. This analysis highlights the healthcare strategies and policy reforms to promote equitable treatment by mitigating these disparities and to improve cholangiocarcinoma outcomes.

Subcutaneous panniculitis-like T-cell lymphoma (SPTCL) is a rare and aggressive cutaneous lymphoma, often misdiagnosed due to nonspecific clinical features. Early diagnosis and treatment remain challenging.

We report the case of a 31-year-old female with a chronic non-healing gluteal wound initially treated as an abscess. The lack of improvement prompted repeated investigations, culminating in the diagnosis of SPTCL with an alpha-beta T-cell phenotype.

Management involved combined chemotherapy and surgical wound reconstruction. Six cycles of CHOEP-21 chemotherapy led to complete clinical remission. A soft tissue defect superinfected with multidrug-resistant organisms was successfully reconstructed using Integra Dermal Regeneration Template followed by split-thickness skin grafting.

This case highlights the diagnostic complexity of SPTCL and the therapeutic potential of dermal matrix application in complex wound management, especially in immuno-compromised patients.