Over the past two decades, experimental and clinical evidence has established the interleukin-23 (IL-23)/interleukin-17 (IL-17) axis as a key mediator of psoriatic inflammation. IL-23, primarily derived from activated dendritic cells, supports the survival and pathogenic function of type 17 immune cells, which subsequently release IL-17A, IL-17F, and IL-22 to promote keratinocyte activation and recruit inflammatory leukocytes. These mechanistic insights have directly translated into the development of highly effective biologic therapies targeting IL-17 or IL-23, substantially improving the management of psoriasis. Beyond injectable biologics, growing efforts to overcome limitations related to long-term adherence, cost, and accessibility have accelerated the development of non-injectable therapeutic approaches. Oral and topical small-molecule agents, including selective tyrosine kinase 2 (TYK2) inhibitors and IL-23 receptor antagonists, are now broadening the therapeutic options. At the same time, progress in molecular engineering, artificial intelligence–guided protein design, and spatial multi-omic technologies are refining therapeutic discovery and enabling more precise targeting of pathogenic immune circuits. In this review, we outline the current understanding of the IL-23/IL-17 pathway in psoriasis pathogenesis and provide a critical overview of approved and emerging therapies directed at this pathway. We also address key biological and translational challenges, including tissue-specific cytokine functions, interspecies differences, and long-term safety considerations, and discuss how these factors may inform future strategies for precision immunotherapy in psoriasis.

Limited data exist regarding the real-world practices and clinical outcomes in patients with ischemic heart failure with reduced left ventricular ejection fractions (LVEFs).Using nationwide registry data from South Korea, we aimed to investigate long-term outcomes and clinical practices, especially implantable cardioverter defibrillators (ICDs) implantation, in patients with reduced LVEFs at least 40 days after acute myocardial infarction (AMI). Of 13,056 patients with AMI between 2011 and 2015, we analyzed 350 (median age, 66 years [interquartile range, 56-75]) who had LVEFs <40% on follow-up transthoracic echocardiogram 40 days after the index event. The primary outcome was cardiac-cause mortality at 3 years. Secondary outcomes comprised major cardiovascular events as well as outcomes defined by the use of ICDs, cardiac resynchronization therapy defibrillators (CRT-Ds), and electrophysiology studies. Among 350 patients, 39 (11.1%) died from cardiac causes during 3 years of follow-up. Eleven (3.1%) were hospitalized for ventricular tachycardia. The rate of ICD or CRT-D implantation up to 3 years was 5.7% (20/350). Cox time-to-event analysis revealed older age, LVEF <30%, diabetes mellitus, and previous MI or revascularization as positively associated with cardiac death, whereas the use of statins and body weight <67 kg were negatively associated. This nationwide Korean registry demonstrated that only 5.7% of patients who had reduced LVEFs after 40 days of AMI underwent ICD implantations over 3 years. Considering the high mortality, concerted efforts are needed to improve clinical outcomes for patients who may have been candidates for ICD implantation.

Chronic rhinosinusitis (CRS) and asthma frequently coexist and represent heterogeneous inflammatory disorders of the upper and lower airways, respectively. Type 2 inflammation, mediated by eosinophils and CD4 T cells, has long been recognized as a central driver of both CRS with nasal polyps (CRSwNP) and asthma pathogenesis. However, emerging evidence underscores the critical roles of innate T cells, such as invariant natural killer T (iNKT), mucosal-associated invariant T (MAIT), and γδ T cells, in airway inflammatory diseases. These innate T cells are enriched in sinonasal tissues and contribute to mucosal inflammation through cytokine production, exhibiting functional polarization that reflects local inflammatory cues. In particular, MAIT17 and Vγ1⁺ γδ T cells have been associated with tissue eosinophilia and disease severity in patients with eosinophilic CRSwNP, whereas iNKT cells display subset-specific distributions across eosinophilic and neutrophilic endotypes. In asthma, iNKT cells consistently contribute to disease development in murine models, whereas the functions of MAIT and γδ T cells remain controversial, showing both pro- and anti-inflammatory effects depending on anatomical location and disease context. This review summarizes current evidence on the contribution of innate T cells to the immunopathology of CRSwNP and asthma and discusses the challenges and future directions in reconciling discrepancies arising from methodological and biological variability.

Idiopathic pulmonary fibrosis (IPF) is characterized by maladaptive epithelial–mesenchymal crosstalk and progressive extracellular matrix accumulation, whereas currently available antifibrotic agents merely decelerate functional decline.This study investigated whether exosomes derived from human mesenchymal stem cells derived from embryonic stem cells (ESC-MSCs) restore epithelial stress responses and attenuate fibrotic remodeling. Human IPF lung transcriptomes were integrated with a bleomycin-induced murine model analyzed by RNA sequencing and protein signaling, together with cigarette smoke extract-induced injury in A549 epithelial cells. ESC-MSCs-derived exosomes exhibited typical morphology and size distribution, enrichment of tetraspanins, and absence of endoplasmic reticulum contamination, consistent with high-purity preparations. Across human IPF and bleomycin-injured lungs, transcriptomic profiling revealed prominent enrichment of extracellular matrix and cytoskeletal gene programs, whereas mitogen-activated protein kinase (MAPK) and Smad families displayed only modest alterations at the mRNA level. In vivo administration of exosomes during the fibrotic remodeling phase, via either intravenous or intratracheal delivery, resulted in improved body weight, reduced lung weight-to-body weight ratios, and decreased collagen deposition and Ashcroft scores. These structural and functional improvements were accompanied by suppression of profibrotic and mesenchymal markers and selective attenuation of activator protein-1 (AP-1) activity. In epithelial injury models, ESC-MSCs-derived exosomes enhanced cell viability, restored redox homeostasis, and constrained stress-induced mesenchymal gene expression and MAPK phosphorylation in both co-treatment and post-treatment settings. Collectively, these data support an epithelial-centered mechanism in which ESC-MSCs-derived exosomes re-establish oxidative balance and selectively restrict AP-1-driven stress signaling, thereby secondarily limiting extracellular matrix accumulation and fibrotic remodeling.

Abrupt vessel closure (AVC) is a complication of percutaneous coronary intervention (PCI) and is defined as the sudden cessation of forward coronary blood flow due to a variety of mechanisms. The incidence of AVC has markedly decreased from approximately 3.0% in the early era to about 0.3% today. Nevertheless, cardiovascular interventionists must remain prepared to manage AVC effectively, given its significant impact on clinical outcomes.AVC can arise from several mechanisms, including dissection, intramural hematoma, intracoronary thrombosis, air embolism, vasospasm, and no-reflow. The clinical impact of AVC varies depending on the extent of myocardium affected, ranging from asymptomatic events or transient ischemic chest pain to cardiogenic shock or cardiac arrest. Both a general approach for stabilizing hemodynamic consequences and an etiology-specific management strategy are essential. Hasty decision-making may worsen the situation, whereas a structured approach—focused on hemodynamic stabilization, logical diagnostic processes, and targeted interventions—can improve outcomes. In this narrative review, we describe the mechanisms underlying each etiology, outline mechanism-specific management strategies, and discuss general approaches to managing patients with AVC through logical diagnostic and treatment processes. We hope this review offers valuable insights into this uncommon but significant complication and enhances readers’ skills in managing AVC more effectively during PCI.

Background: Although patients with malignant melanoma in situ (MIS) have a high survival rate, a risk of recurrence or upstaging remains. Thus, a comprehensive understanding of its prognosis is essential for optimal patient management. Objective: To investigate the clinical characteristics and survival outcomes of Korean patients with MIS. Methods: We retrospectively analyzed the medical records and photographs of patients with MIS treated at a single tertiary center between 2008 and 2021. Clinical features, including diagnosis, treatment, recurrence, and mortality, were examined. Results: A total of 156 patients with MIS were included, with a mean age of 59.3 years. The most common subtype was acral lentiginous melanoma (80.8%). Delayed diagnosis was associated with subungual MIS (SUMis; p ＜0.05). Among the subtypes other than SUMis, 77.3% met three or more of the ABCD criteria for melanoma.Hutchinson’s sign was observed in 67.3% of cases of SUMis. Ulceration was present in only two cases (1.3%).Recurrence occurred in nine patients (5.8%), with four (2.6%) experiencing relapse after 5 years. Upstaging was observed in two patients (1.3%) due to intralymphatic or regional nodal metastasis occurring at 19 and 10 months post-treatment. The 5-year and 10-year melanoma-specific/overall survival rates were 100.0/96.9% and 100.0/89.0%, respectively. Conclusion Although the survival rates of patients with MIS are high, long-term and close follow-up after treatment is essential because of the possibility of late recurrence and rare instances of intralymphatic or regional nodal metastasis. Additionally, the presence of clinical ulceration is highly suggestive of invasive melanoma.

Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

Background and Objectives: Among various emerging catheter-based treatments for severe tricuspid regurgitation (TR), the spacer device can reduce the regurgitation orifice without manipulating the valve leaflet. However, its clinical application has been hampered by traumatic anchoring to the myocardium and the coaxial alignment of the balloon resulting in insufficient TR reduction. This study aimed to evaluate the early-stage safety, technical feasibility, and preliminary efficacy of the novel atraumatic vertical spacer in patients with isolated severe TR. Methods: All procedures were guided by fluoroscopy and transthoracic echocardiography.The maximum device placement time with an inflated balloon was 24 hours. Changes in the amount of TR, right ventricular function, and patient hemodynamics were measured during balloon deployment. Results: A total of 7 patients (median age 74), underwent successful device implantation without procedure-related complications. During balloon inflation (median 25 minutes), there were no symptoms or signs indicative of TR intolerance. TR was reduced by 1 grade or greater in all patients, with 2 patients exhibiting a reduction of 3 grades, from torrential TR to a moderate degree. Mild TR after balloon inflation was achieved in 3 patients with baseline severe TR. The TR reduction observed during initial balloon deployment was sustained during the subsequent balloon maintenance period. Conclusions The Pivot-balloon procedure was safe, technically feasible, and effective in reducing TR in patients with severe TR. No periprocedural complications or adverse cardiovascular events were reported during device placement with TR reduction observed in all patients. However, longer-term follow-up is needed to confirm safety and treatment effect.

Background and Objectives: Cigarette smoking is a major risk factor for atherosclerosis.Nicotine, a crucial constituent of tobacco, contributes to atherosclerosis development and progression. However, evidence of the association between nicotine and neointima formation is limited. We aimed to evaluate whether nicotine enhances neointimal hyperplasia in the native epicardial coronary arteries of pigs after percutaneous coronary intervention (PCI) with drug-eluting stents (DES). Methods: After coronary angiography (CAG) and quantitative coronary angiography (QCA), we implanted 20 DES into 20 pigs allocated to 2 groups: no-nicotine (n=10) and nicotine (n=10) groups. Post-PCI CAG and QCA were performed immediately. Follow-up CAG, QCA, optical coherence tomography (OCT), and histopathological analyses were performed 2 months post-PCI. Results: Despite intergroup similarities in the baseline QCA findings, OCT analysis showed that the nicotine group had a smaller mean stent and lumen areas, a larger mean neointimal area, greater percent area stenosis, and higher peri-strut fibrin and inflammation scores than the no-nicotine group. In immunofluorescence analysis, the nicotine group displayed higher expression of CD68 and α-smooth muscle actin but lower CD31 expression than the no-nicotine group. Conclusions Nicotine inhibited re-endothelialization and promoted inflammation and NIH after PCI with DES in a porcine model.

Background: Despite the critical importance of sleep medicine within neurology, notable gaps in education and clinical practice persist among neurologists. This study aims to explore the extent of involvement and the challenges faced by Korean neurologists in sleep medicine, focusing on awareness of polysomnography training program, the operation of sleep study facilities, and educational exposure. Methods: An online survey collected responses from 233 neurologists, focusing on their demographics, knowledge of and involvement in sleep medicine, operation of sleep study facilities, and participation in residency training. Results: The findings indicated that 84.9% of neurologists were aware of polysomnography training program, primarily through professional societies. Nonetheless, 15.1% reported unfamiliarity with these initiatives, with 72.7% of this subgroup expressing interest in sleep medicine yet lacking access to information. In terms of clinical practice, 74 neurologists operated sleep study facilities, with 63% intending to expand. Key operational challenges included staff management, maintaining patient volumes, and inadequate institutional support. Among respondents from teaching hospitals, only 36 out of 114 reported active resident involvement in sleep study interpretations, predominantly hindered by excessive workloads and insufficient staffing. Conclusions A significant number of neurologists have an interest in sleep medicine; however, substantial challenges impede effective education and clinical practice. These results underscore the need for improved educational resources and institutional support to enhance the growth and effectiveness of sleep medicine practices among neurologists.