Phenotypic & Molecular Insights into Carbapenem-Resistant E. coli in Retail Meats | Thailand Study #pencis #researchawards

Introduction

Carbapenem-resistant Escherichia coli (CREC) has emerged as a critical public health concern due to its resistance to last-resort antibiotics and its increasing detection outside hospital settings. The presence of CREC in retail meats represents a potential pathway for transmission of antimicrobial resistance from food-producing animals to humans. Understanding the occurrence, resistance mechanisms, and genetic characteristics of CREC in food sources is essential for risk assessment and the development of effective surveillance and control strategies, particularly in regions where antimicrobial use in animal production is common.

Prevalence of Carbapenem-Non-Susceptible E. coli in Retail Meats

The investigation demonstrated a high prevalence of presumptive carbapenem-non-susceptible E. coli (CNSEC) in retail meat samples, with beef showing the highest contamination rate. The large proportion of CNSEC isolates subsequently confirmed as CREC highlights retail meat as a significant reservoir of carbapenem-resistant bacteria. These findings suggest that the food chain may play an underrecognized role in the dissemination of carbapenem resistance, emphasizing the need for systematic monitoring of antimicrobial resistance in meat products.

Phenotypic Antimicrobial Resistance Profiles

Phenotypic susceptibility testing revealed that a substantial proportion of isolates exhibited resistance to both imipenem and meropenem, confirming their classification as CREC. The high level of resistance observed across different meat types underscores the limited therapeutic options available for infections caused by these strains. Such phenotypic resistance patterns also raise concerns about selective pressure from antimicrobial use in livestock, which may contribute to the maintenance and spread of highly resistant E. coli populations.

Molecular Detection of Carbapenemase Genes

Molecular analysis showed that only a small percentage of CREC isolates carried carbapenemase genes, predominantly the blaNDM gene, with one isolate also harboring blaVIM. Although the prevalence of these genes was low, their presence is alarming because blaNDM is associated with rapid global dissemination and high-level resistance. The detection of these genes in food-associated isolates indicates the potential for horizontal gene transfer and highlights the importance of molecular surveillance alongside phenotypic testing.

Virulence Factors and Phylogenetic Characteristics

All carbapenemase-positive CREC isolates carried the fimH gene, a key adhesion factor involved in colonization, but lacked other major virulence determinants. Phylogenetic analysis classified these isolates within Group D, which is often associated with extraintestinal pathogenic E. coli. This combination of antimicrobial resistance and phylogenetic background suggests that even isolates with limited virulence gene profiles may still pose a risk if they acquire additional pathogenic traits or are transmitted to vulnerable populations.

Public Health Implications and Research Perspectives

The identification of CREC carrying clinically important resistance genes in retail meats has significant implications for food safety and public health. These findings reinforce the need for a One Health approach integrating human, animal, and environmental surveillance of antimicrobial resistance. Future research should focus on tracking transmission pathways, assessing the role of food handling and preparation practices, and evaluating interventions to reduce the emergence and spread of carbapenem-resistant bacteria within the food supply chain.

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#CarbapenemResistance, #CREC, #AntimicrobialResistance, #FoodSafetyResearch, #OneHealth, #EscherichiaColi, #RetailMeatSurveillance, #blaNDM, #CarbapenemaseGenes, #MolecularEpidemiology, #PublicHealthMicrobiology, #ZoonoticRisk, #AMRResearch, #PhylogeneticAnalysis, #VirulenceFactors, #FoodbornePathogens, #GlobalHealthThreat, #ThailandResearch, #ClinicalMicrobiology, #InfectiousDiseaseResearch,

Mucocutaneous Eruption Children | Mycoplasma pneumoniae Clinical & Immunological #researchawards

Introduction

Reactive infectious mucocutaneous eruption (RIME) is an emerging pediatric mucocutaneous syndrome characterized by prominent mucositis with limited or absent skin involvement and an infectious, rather than drug-induced, etiology. First distinguished from Stevens–Johnson syndrome (SJS), RIME poses diagnostic challenges due to overlapping clinical features. Mycoplasma pneumoniae is the most frequently implicated pathogen, particularly in children, where recognition is critical to avoid misdiagnosis and inappropriate management. Understanding RIME as a distinct clinical entity has significant implications for diagnosis, treatment, and prognosis in pediatric infectious diseases and dermatology research.

Etiopathogenesis and Infectious Triggers

Current evidence highlights M. pneumoniae as the predominant trigger of RIME, with pathogenesis believed to involve immune-mediated mechanisms rather than direct pathogen invasion. Molecular mimicry and immune complex formation are hypothesized contributors to mucosal injury. Recent literature has expanded the spectrum of infectious triggers to include viral and bacterial pathogens, emphasizing RIME as a post-infectious immunologic phenomenon. Research into host susceptibility, immune pathways, and pathogen-specific responses remains crucial to elucidate disease mechanisms.

Clinical Spectrum and Phenotypic Variability

RIME demonstrates marked clinical heterogeneity, ranging from isolated mucositis to multisite involvement of oral, ocular, and genital mucosa, with minimal or variable cutaneous findings. This variability complicates early diagnosis and contributes to confusion with SJS or erythema multiforme. Pediatric case series, including the described male patients aged 2–12 years, illustrate presentations from absent skin lesions to widespread rash, underscoring the need for phenotype-based clinical classification in future research.

Diagnostic Challenges and Differential Diagnosis

Differentiating RIME from SJS is a central clinical and research challenge due to overlapping mucocutaneous features but divergent etiologies and prognoses. Accurate diagnosis relies on thorough clinical assessment, exclusion of drug triggers, and confirmation of infectious etiology through serology or PCR. Research efforts should focus on developing standardized diagnostic criteria and biomarkers to facilitate early recognition and reduce misclassification in both clinical practice and epidemiologic studies.

Management Strategies and Therapeutic Outcomes

Management of RIME is largely supportive and multidisciplinary, involving antimicrobial therapy targeting M. pneumoniae, mucosal care, and systemic treatment for complications such as pneumonia or sepsis. The favorable recovery observed within 10–21 days in reported cases supports the effectiveness of timely intervention. However, variability in disease severity and recurrence highlights the need for clinical trials and consensus guidelines to optimize therapeutic strategies and long-term follow-up.

Prognosis, Recurrence, and Research Implications

Although generally associated with good outcomes, RIME can exhibit a relapsing phenotype, as demonstrated by recurrent hospitalizations in some patients. Long-term sequelae, including post-inflammatory hyperpigmentation or ocular complications, warrant further investigation. From a research perspective, RIME represents an important model of infection-triggered mucocutaneous disease, emphasizing the need for multicenter studies to define epidemiology, recurrence risk, and preventive strategies in pediatric populations.

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#ReactiveInfectiousMucocutaneousEruption, #RIME, #MycoplasmaPneumoniae, #PediatricDermatology, #PediatricInfectiousDiseases, #Mucositis, #ExtraPulmonaryManifestations, #StevensJohnsonSyndrome, #ClinicalResearch, #RareDiseases, #ImmuneMediatedDisease, #PediatricCaseSeries, #InfectiousTriggers, #DiagnosticChallenges, #MultidisciplinaryCare, #RelapsingDisease, #ClinicalPhenotypes, #MucocutaneousDisorders, #TranslationalResearch, #PediatricImmunology,

Two-Time Longitudinal Assessment of Healthcare Workers’ COVID-19 Exposure #pencis #researchawards

Introduction

Healthcare workers (HCWs) have been at the forefront of the COVID-19 pandemic and have faced prolonged occupational exposure to SARS-CoV-2. Despite widespread implementation of infection prevention and control (IPC) measures, the persistence of the pandemic and its transition into more routine phases have raised concerns about sustained exposure risks and behavioral fatigue. Understanding how occupational and community exposure risks evolve over time, along with adherence to IPC practices, is essential for protecting HCWs and maintaining healthcare system resilience. This study addresses an important gap by prospectively examining exposure risks and IPC adherence among HCWs beyond the acute pandemic phase.

Study Design and Setting

This prospective observational study was conducted across four public hospitals in the Thessaly region of Greece, providing a representative snapshot of HCWs operating in diverse clinical environments. Data collection occurred at two time points—baseline (January–March 2022) and a six-month follow-up—allowing for temporal comparisons. By focusing on HCWs who reported contact with suspected or confirmed COVID-19 cases, the study targeted individuals with meaningful exposure risk, thereby strengthening the relevance of its findings to real-world clinical practice.

Assessment of Occupational and Community Exposure

Exposure risk was systematically evaluated using the World Health Organization’s standardized risk assessment questionnaire for HCWs. This instrument captured both occupational exposure, such as patient contact during routine care or aerosol-generating procedures, and community exposure outside the workplace. The consistent finding that nearly three-quarters of participants reported occupational exposure at both time points underscores the sustained nature of risk for HCWs, even as pandemic dynamics evolved.

Temporal Changes in Risk Classification

Among HCWs with occupational exposure, a significant increase in high-risk classification was observed over time, rising from 76% at baseline to 88% at follow-up. This shift indicates that although the proportion of exposed HCWs remained stable, the intensity or quality of exposure worsened. The more than twofold increase in odds of being classified as high-risk highlights a substantial effect size and suggests growing vulnerability, potentially linked to cumulative exposure, changes in work practices, or declining vigilance.

Professional Role and Differential Risk

The study revealed notable differences in exposure risk by professional role, with nurses consistently demonstrating higher risk compared with physicians. This disparity likely reflects the nature of nursing duties, which involve more frequent and prolonged patient contact, including close bedside care. These findings emphasize the need for role-specific risk mitigation strategies and targeted support for professional groups disproportionately affected by occupational exposure.

Adherence to Infection Prevention and Control Practices

While overall use of personal protective equipment (PPE) remained high throughout the study period, adherence to several critical IPC practices declined over time. Specifically, proper removal and replacement of PPE and routine decontamination of high-touch surfaces were less consistently followed at follow-up. This decline may reflect pandemic fatigue or normalization of risk, underscoring the importance of continuous training, monitoring, and reinforcement of IPC measures to sustain protective behaviors among HCWs.

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#COVID19Research #HealthcareWorkers #OccupationalExposure #InfectionPrevention #IPCPractices #PandemicFatigue #ProspectiveStudy #HospitalEpidemiology #PublicHealthResearch #SARSCoV2 #PPECompliance #AerosolGeneratingProcedures #RiskAssessment #NursingResearch #PhysicianSafety #WorkplaceHealth #EpidemiologyStudy #HealthcareSafety #WHOGuidelines #PostPandemicCare

Tai Chi on Exercise Capacity and Quality of Life in Chronic Heart Failure #pencis #researchawards

Introduction

Chronic heart failure (CHF) remains a major global health burden, characterized by reduced exercise tolerance, impaired quality of life (QoL), and high healthcare utilization. Alongside conventional pharmacological and device-based therapies, non-pharmacological interventions such as cardiac rehabilitation play a crucial role in CHF management. Tai Chi (TC), a traditional mind–body exercise combining slow movements, controlled breathing, and mental focus, has gained attention as a potentially safe and accessible rehabilitation strategy for CHF patients. However, its clinical efficacy remains debated, necessitating evidence-based evaluation.

Rationale for Tai Chi in Cardiac Rehabilitation

Tai Chi is considered a low-to-moderate intensity aerobic exercise, making it suitable for older adults and patients with limited physical capacity, such as those with CHF. Its emphasis on balance, relaxation, and gentle movement may reduce sympathetic activation and improve psychosocial well-being. From a research perspective, TC offers a holistic intervention that may complement standard cardiac rehabilitation, particularly for patients unable or unwilling to engage in conventional exercise programs.

Methodological Approach of the Meta-Analysis

The meta-analysis synthesized evidence from randomized controlled trials (RCTs) evaluating TC in CHF patients with reduced left ventricular ejection fraction (≤45%). Comprehensive searches of PubMed and EMBASE databases ensured systematic identification of eligible studies. By calculating weighted mean differences (WMDs) and assessing heterogeneity using the I² statistic, the analysis aimed to quantitatively determine the impact of TC on functional capacity, biomarkers, hemodynamic parameters, and QoL outcomes.

Effects of Tai Chi on Quality of Life

One of the most consistent findings of the meta-analysis was the significant improvement in QoL among CHF patients practicing Tai Chi. The observed reduction in QoL scores suggests meaningful psychosocial and functional benefits, potentially mediated through reduced stress, enhanced self-efficacy, and improved emotional well-being. These findings highlight QoL as a sensitive outcome measure for mind–body interventions and underscore TC’s value beyond purely physiological endpoints.

Impact on Exercise Capacity and Clinical Outcomes

Despite favorable effects on QoL, Tai Chi did not demonstrate statistically significant improvements in objective clinical parameters such as N-terminal pro-brain natriuretic peptide levels, blood pressure, peak oxygen uptake, or six-minute walking distance. While trends toward improved exercise capacity were observed, the lack of significance may reflect limited sample sizes, short intervention durations, or variability in TC protocols across studies.

Research Gaps and Future Directions

The current evidence base is constrained by small-scale RCTs and methodological heterogeneity, limiting definitive conclusions regarding Tai Chi’s role in CHF management. Future research should prioritize larger, well-designed trials with standardized TC interventions, longer follow-up periods, and integration of both clinical and patient-reported outcomes. Such studies are essential to clarify whether Tai Chi can influence disease progression, functional capacity, and long-term prognosis in CHF patients.

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#ChronicHeartFailure #TaiChiResearch #CardiacRehabilitation #MetaAnalysis #QualityOfLife #ExerciseTherapy #MindBodyMedicine #HeartFailureManagement #ClinicalResearch #RCTs #NonPharmacologicalTherapy #EvidenceBasedMedicine #CardiovascularHealth #RehabilitationScience #PatientCenteredCare #ExerciseCapacity #HeartFailureStudies #IntegrativeMedicine #HealthOutcomes #FutureResearch

Decoding the Complexity of IgA Immune Responses Respiratory Syncytial Virus #pencis #researchawards

Introduction

Respiratory syncytial virus (RSV) remains one of the most significant viral threats to infant respiratory health worldwide, causing severe lower respiratory tract infections that can lead to hospitalization and long-term pulmonary complications. Despite decades of research, effective and durable protective strategies for early life remain elusive, largely due to fundamental age-dependent differences in immune function. Infants exhibit distinct mucosal immune responses compared to adults, particularly at the level of antibody production and immune regulation. Understanding how these developmental differences influence susceptibility to RSV is critical for advancing vaccine development and improving clinical outcomes in this vulnerable population.

Age-Dependent Mucosal Immunity in RSV Infection

Mucosal immunity in the respiratory tract undergoes profound developmental changes from infancy to adulthood, shaping host defense against RSV. In infants, immune responses are biased toward tolerance and immune regulation, a feature thought to protect against excessive inflammation during early microbial exposure. However, this bias results in diminished antiviral effector responses, including reduced antibody production at mucosal surfaces. These age-specific immune characteristics contribute to higher viral replication, prolonged infection, and increased disease severity in infants compared to adults during RSV infection.

Role of IgA in Controlling RSV at Respiratory Surfaces

Immunoglobulin A (IgA) is the predominant antibody isotype at respiratory mucosal surfaces and serves as a first line of defense against RSV by neutralizing the virus and limiting epithelial infection. In adults, robust RSV-specific IgA responses correlate with reduced viral load and milder disease. In contrast, infants exhibit markedly reduced IgA production following RSV exposure. This deficiency compromises mucosal barrier protection and facilitates viral persistence, highlighting IgA as a critical but underdeveloped component of early-life immunity against RSV.

Impaired Class Switch Recombination in Infant B Cells

The failure of infants to generate strong IgA responses during RSV infection is closely linked to impaired class switch recombination (CSR) in B cells. Neonatal B cells display intrinsic limitations in undergoing CSR due to reduced expression of key activation-induced cytidine deaminase (AID) and altered signaling through cytokine and costimulatory pathways. These molecular constraints limit the diversification of antibody isotypes, skewing responses toward less effective humoral immunity and reinforcing susceptibility to severe RSV disease in early life.

Regulatory B Cells as Modulators of Antiviral Immunity

Regulatory B cells (Bregs), particularly neonatal Bregs (nBregs), have emerged as critical modulators of immune responses during infancy. These cells exert immunosuppressive effects through cytokine production, such as interleukin-10, dampening antiviral T-cell responses and inhibiting effective B-cell activation. During RSV infection, nBregs can suppress class switch recombination and IgA production, thereby limiting protective mucosal immunity. While this regulatory function may prevent immunopathology, it paradoxically contributes to increased viral burden and disease severity in infants.

Implications for Infant-Specific RSV Vaccine Design

Elucidating the mechanisms underlying impaired IgA responses and Breg-mediated immune suppression has profound implications for RSV vaccine development. Traditional vaccine strategies designed for adults may fail in infants due to their unique immune regulatory environment. Targeted approaches that enhance mucosal IgA production, modulate Breg activity, or promote age-appropriate B-cell maturation may offer more effective protection. A deeper understanding of infant-specific immune pathways is essential for the rational design of next-generation RSV vaccines and immunomodulatory interventions tailored to early life.

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#RSVResearch, #InfantImmunity, #MucosalImmunity, #IgAResponse, #RespiratoryViruses, #NeonatalImmunity, #BCellBiology, #RegulatoryBCells, #RSVVaccines, #PediatricInfections, #AntiviralImmunity, #ImmuneDevelopment, #EarlyLifeImmunity, #ClassSwitchRecombination, #RespiratoryHealth, #ViralPathogenesis, #Immunoregulation, #VaccineDesign, #TranslationalImmunology, #PediatricResearch

Reveals Defense Pathways in Chinese Cabbage Against Black Spot Disease 🌱🧬 #pencis #researchawards

Introduction

Black spot disease, caused by Alternaria brassicicola, represents a major biotic constraint to Chinese cabbage production, leading to significant yield and quality losses. Understanding the molecular and biochemical defence strategies employed by resistant germplasm is essential for developing durable disease management approaches. Recent advances in multi-omics technologies have enabled integrated analyses of transcriptomic and metabolomic responses during early pathogen infection, offering new insights into host–pathogen interactions. In this context, the Chinese cabbage line 904B provides an excellent model to dissect early defence signalling and resistance-associated pathways against black spot disease.

Hormonal Reprogramming During Early Infection

Upon infection with A. brassicicola, Chinese cabbage line 904B exhibits a pronounced shift in phytohormone signalling. Growth-related hormones such as cytokinin and auxin are significantly suppressed, reflecting a strategic reallocation of resources away from development toward defence. In contrast, defence-associated hormones, particularly ethylene and jasmonic acid (JA), are strongly activated. This hormonal reprogramming highlights the central role of JA–ethylene crosstalk in mediating resistance to necrotrophic pathogens and underscores the importance of hormone balance in early immune responses.

Transcriptomic Insights Into Defence Activation

Transcriptomic profiling at 24 hours post-inoculation reveals extensive gene expression reprogramming in 904B. Genes involved in signal transduction, reactive oxygen species (ROS) production, and stress responses are markedly upregulated, while those associated with cell growth and differentiation are downregulated. Notably, defence-related kinases and transcriptional regulators show rapid induction, suggesting a tightly controlled signalling cascade that enables rapid perception of pathogen invasion and activation of downstream immune responses.

Metabolomic Remodeling and Secondary Metabolites

Metabolomic analysis demonstrates significant alterations in secondary metabolite accumulation following pathogen challenge. Among these, the sterol compound 4,4-dimethyl-5α-cholest-7-en-3β-ol is markedly upregulated in infected tissues, implicating sterol metabolism in plant defence. Differentially accumulated metabolites are primarily enriched in indole alkaloid metabolism and glycerolipid metabolism pathways, indicating their involvement in strengthening cellular barriers, modulating membrane integrity, and enhancing antimicrobial activity during black spot disease resistance.

Functional Role of BraPBL in Disease Resistance

BraPBL, a receptor-like cytoplasmic kinase (RLCK) family member, exhibits progressively increased expression with prolonged A. brassicicola infection. Functional analyses demonstrate that overexpression of BraPBL significantly enhances resistance to black spot disease, whereas gene silencing compromises host defence. Subcellular localization studies confirm that BraPBL resides at the plasma membrane, consistent with its proposed role in early pathogen perception and signal initiation.

BraPBL-Mediated Signalling and Defence Pathways

Overexpression of BraPBL leads to the activation of key defence-associated genes, including the ROS-generating enzyme RBOH and the mitogen-activated protein kinase kinase kinase MEKK1. This activation promotes ROS accumulation and signal amplification, while simultaneously stimulating the JA signalling pathway. Collectively, these findings position BraPBL as a crucial positive regulator of black spot disease resistance, linking membrane-associated signalling, hormone-mediated defence, and metabolic reprogramming in Chinese cabbage.

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#BlackSpotDisease, #ChineseCabbage, #AlternariaBrassicicola, #PlantPathology, #PlantImmunity, #Transcriptomics, #Metabolomics, #Phytohormones, #JasmonicAcid, #EthyleneSignaling, #SecondaryMetabolites, #SterolMetabolism, #BraPBL, #RLCK, #ROS, #MAPKSignaling, #DiseaseResistance, #HostPathogenInteraction, #PlantDefenseMechanisms, #CropProtection

Liver Crossroads🧬| Orchestrating Lipoprotein Dynamics & Lipid Homeostasis #pencis #researchawards

Introduction

The liver is a central metabolic organ responsible for maintaining systemic lipid homeostasis through tightly regulated processes such as fatty acid uptake, oxidation, and the assembly and secretion of very low-density lipoproteins (VLDLs). These pathways allow the liver to detoxify excess circulating free fatty acids and redistribute lipids to peripheral tissues for energy utilization. Disruption of these mechanisms contributes to hepatic lipid accumulation and the development of metabolic dysfunction-associated steatotic liver disease (MASLD), previously termed non-alcoholic fatty liver disease (NAFLD). Given the close association between hepatic lipid dysregulation, cardiovascular disease, and metabolic disorders, understanding liver lipid metabolism remains a major focus of biomedical research.

Hepatic Fatty Acid Uptake and Intracellular Trafficking

Hepatic fatty acid uptake occurs through both passive diffusion and transporter-mediated mechanisms involving proteins such as CD36 and fatty acid transport proteins (FATPs). Once inside hepatocytes, fatty acids are esterified, oxidized, or incorporated into lipoproteins. Intracellular trafficking of fatty acids toward mitochondria, peroxisomes, or the endoplasmic reticulum is tightly regulated to prevent lipotoxicity. Dysregulation at this stage can shift lipid flux toward storage rather than oxidation, promoting hepatic steatosis and metabolic stress, making this process a critical area for mechanistic and translational research.

Fatty Acid Oxidation and Hepatic Energy Homeostasis

Fatty acid oxidation is essential for maintaining hepatic energy balance and preventing lipid overload. Mitochondrial β-oxidation serves as the primary pathway for fatty acid catabolism, while peroxisomal oxidation handles very-long-chain fatty acids. Impairment in these oxidative pathways leads to lipid accumulation, mitochondrial dysfunction, oxidative stress, and inflammation—hallmarks of MASLD progression. Current research focuses on transcriptional regulators such as PPARα and AMPK, which coordinate fatty acid oxidation and represent potential therapeutic targets.

VLDL Biogenesis: Molecular Assembly and Lipidation

VLDL biogenesis is a multistep process initiated in the endoplasmic reticulum, where apolipoprotein B100 (ApoB100) is lipidated by microsomal triglyceride transfer protein (MTP). This process ensures efficient packaging of triglycerides and cholesterol into nascent lipoprotein particles. Defects in VLDL assembly can result in intracellular triglyceride accumulation, exacerbating hepatic steatosis. Despite its importance, the precise regulation of ApoB stability, lipid availability, and ER quality control during VLDL formation remains incompletely understood.

Regulation of VLDL Secretion and Systemic Lipid Distribution

Once assembled, VLDLs are secreted into the circulation to deliver triglycerides to peripheral tissues. This secretion process plays a protective role by exporting excess hepatic lipids; however, excessive VLDL output contributes to hypertriglyceridemia and atherosclerosis. Hormonal signals, nutrient availability, and insulin resistance strongly influence VLDL secretion rates. Ongoing research aims to clarify how altered hepatic insulin signaling selectively enhances VLDL secretion while failing to suppress lipid synthesis in metabolic disease states.

Clinical Implications and Future Research Directions

Dysregulation of fatty acid oxidation and VLDL metabolism links MASLD to systemic metabolic disorders, including type 2 diabetes and cardiovascular disease. Given that atherosclerosis remains the leading cause of global mortality, hepatic lipid handling has emerged as a critical determinant of cardiometabolic risk. Future research must integrate molecular biology, omics technologies, and clinical studies to unravel unresolved mechanisms governing hepatic lipid balance. Advancing this knowledge is essential for developing targeted therapies to prevent liver disease progression and reduce cardiovascular morbidity.

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#LiverMetabolism #VLDL #FattyAcidOxidation #LipidHomeostasis #MASLD #NAFLD #HepaticSteatosis #CardiometabolicHealth #Atherosclerosis #MetabolicDisease #ApoB100 #MTP #InsulinResistance #LipidResearch #Hepatology #MolecularMetabolism #TranslationalResearch #CardiovascularRisk #MetabolicSyndrome #LiverHealth