Biological heart age estimation offers valuable insights into the aging process of the heart. Although, existing research does not differentiate the age-related changes within the heart's various regions.
Determine the biological age of the left ventricle (LV), right ventricle (RV), myocardium, left atrium, and right atrium via magnetic resonance imaging radiomics phenotypes, and explore factors influencing aging specific to each cardiac region.
The study utilized a cross-sectional methodology.
The UK Biobank study encompassed 18,117 healthy participants, detailed as 8,338 men (mean age 64.275 years) and 9,779 women (mean age 63.074 years).
Steady-state free precession, balanced, at 15T.
Segmentation of five cardiac regions was achieved using an automated algorithm, which subsequently facilitated the extraction of radiomic features. Using radiomics features as predictors and chronological age as the output variable, Bayesian ridge regression was employed to calculate the biological age for each cardiac region. The gap in age represented the variance between biological and chronological measurements of age. To determine associations between age disparities in cardiac regions and socioeconomic factors, lifestyle, body composition, blood pressure, arterial stiffness, blood biomarkers, mental well-being, multi-organ health, and sex hormone exposures, linear regression was applied (n=49).
False discovery rate correction, with a 5% threshold, was used to adjust the multiple testing outcomes.
The model's estimations for RV age displayed the largest discrepancy from the actual value, whereas estimations for LV age exhibited the smallest error. The mean absolute error was 526 years in men for RV and 496 years for LV. Age gaps, statistically significant, numbered 172 in the observed associations. Greater abdominal fat deposition displayed the strongest correlation with larger age disparities, including variations in myocardial age among females (Beta=0.85, P=0.0001691).
Large age gaps, for example, are linked to poor mental health, marked by episodes of disinterest and myocardial age discrepancies in men (Beta=0.25, P=0.0001). A history of dental problems, such as left ventricular hypertrophy in men (Beta=0.19, P=0.002), is similarly associated. The strongest association observed was between higher bone mineral density and smaller myocardial age gaps in men, as evidenced by the beta coefficient of -152 and a p-value of 74410.
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By employing image-based heart age estimation, a novel approach, this work contributes to a deeper understanding of cardiac aging.
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In tandem with industrial development, a number of chemicals have emerged, with endocrine-disrupting chemicals (EDCs) standing out as crucial to plastic production, where they function as both plasticizers and flame retardants. Plastics' ubiquity in modern life is tied to their ease of use, which, however, results in greater human exposure to endocrine-disrupting chemicals. Endocrine disruption by EDCs leads to adverse effects like reproductive failure, cancerous growths, and neurological anomalies, marking them as dangerous substances. Moreover, these substances are harmful to a multitude of organs, yet they persist in use. Subsequently, evaluating EDCs' contamination status, identifying potentially hazardous substances for management, and monitoring safety standards are vital. Correspondingly, it is important to discover substances that can protect against EDC toxicity and actively study the protective impact of these compounds. Korean Red Ginseng (KRG) is found, in recent research, to exhibit protective effects against multiple toxicities caused in humans by exposure to EDCs. This review examines the impact of endocrine-disrupting chemicals (EDCs) on the human organism, along with the protective function of the keratinocyte growth regulation (KRG) pathway in mitigating EDC toxicity.
Psychiatric disorders can be ameliorated by red ginseng (RG). The alleviation of stress-induced gut inflammation is facilitated by fermented red ginseng (fRG). Gut inflammation, coupled with gut dysbiosis, can lead to psychiatric disorders. In mice, we investigated the gut microbiota's role in the anxiety/depression-reducing effects of RG and fRG, by evaluating the impact of RG, fRG, ginsenoside Rd, and 20(S),D-glucopyranosyl protopanaxadiol (CK) on AD and colitis triggered by gut microbiota dysbiosis.
Mice concurrently afflicted with AD and colitis were subjected to either immobilization stress or fecal matter transplant from patients exhibiting ulcerative colitis and depression. AD-like behaviors were assessed using the elevated plus maze, light/dark transition, forced swimming, and tail suspension tests as methods of evaluation.
The oral gavage of UCDF in mice was associated with an increase in AD-like behaviors, as well as the development of neuroinflammation, gastrointestinal inflammation, and modifications to the gut microbial community. Oral treatment with fRG or RG lessened the behavioral effects of UCDF associated with Alzheimer's disease, reduced interleukin-6 production in the hippocampus and hypothalamus, lowered blood corticosterone, whereas UCDF reduced expression of hippocampal brain-derived neurotrophic factor.
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A surge was observed in the cell population, alongside elevated levels of dopamine and hypothalamic serotonin. Furthermore, UCDF-induced colonic inflammation was reduced by their treatments, and the disturbance of the UCDF-induced gut microbiota was partially recovered by their treatments. fRG, RG, Rd, or CK, when administered orally, alleviated IS-induced AD-like behaviors by reducing blood IL-6 and corticosterone, colonic IL-6 and TNF, and mitigating gut dysbiosis. A corresponding increase in suppressed hypothalamic dopamine and serotonin levels occurred.
Mice subjected to oral UCDF gavage presented with AD, neuroinflammation, and gastrointestinal inflammation. fRG's influence on AD and colitis in UCDF-exposed mice relied on the regulation of the microbiota-gut-brain axis, whereas in IS-exposed mice, the regulation of the hypothalamic-pituitary-adrenal axis was instrumental.
In mice, oral UCDF administration resulted in the appearance of AD, neuroinflammation, and gastrointestinal inflammation. fRG alleviated AD and colitis in UCDF-exposed mice through modulation of the microbiota-gut-brain axis, and in IS-exposed mice through modulation of the hypothalamic-pituitary-adrenal axis.
Myocardial fibrosis (MF), a serious and advanced pathological consequence of a multitude of cardiovascular diseases, is a significant risk factor for heart failure and malignant arrhythmias. Still, the current therapies for MF remain without the inclusion of any specific medicinal drugs. Although ginsenoside Re demonstrates an anti-MF effect in rats, the mechanistic details remain obscure. In order to investigate the anti-MF effects of ginsenoside Re, we developed a mouse model of acute myocardial infarction (AMI) and an in vitro model of Ang II-induced cardiac fibroblasts (CFs).
The anti-MF effect of miR-489 in CFs was probed by the introduction of miR-489 mimic and inhibitor via transfection. The impact of ginsenoside Re on MF and its associated mechanisms was explored using ultrasonography, ELISA, histopathological staining, transwell assays, immunofluorescence, Western blotting, and qPCR in a mouse model of AMI and an Ang-induced CFs model.
A consequence of MiR-489 treatment in normal and Ang-treated CFs was a reduction in the expression of -SMA, collagen, collagen and myd88, and a resultant inhibition of NF-κB p65 phosphorylation. VX-770 Ginsenoside Re's potential to improve cardiac function is linked to its ability to restrain collagen accumulation and cardiac fibroblast migration, alongside stimulating miR-489 transcription and reducing myd88 expression and NF-κB p65 phosphorylation.
MiR-489 effectively curtails the pathological progression of MF, its mechanism at least partially stemming from modulation of the myd88/NF-κB pathway. The amelioration of AMI and Ang-induced MF by Ginsenoside Re likely involves, at least in part, the regulation of the miR-489/myd88/NF-κB signaling pathway. VX-770 Consequently, miR-489 could serve as a potential therapeutic target for anti-MF agents, while ginsenoside Re emerges as a promising medication for MF treatment.
The pathological process of MF is effectively inhibited by MiR-489, and a key component of this mechanism, at least partially, involves regulation of the myd88/NF-κB pathway. Ginsenoside Re's ability to alleviate AMI and Ang-induced MF is at least partly due to its role in modulating the miR-489/myd88/NF-κB signaling pathway. Thus, miR-489 may be a suitable focus for anti-MF approaches, and ginsenoside Re might prove a helpful medication for managing MF.
QiShen YiQi pills (QSYQ), a Traditional Chinese Medicine (TCM) preparation, have a marked influence on the treatment of myocardial infarction (MI) patients within clinical practice. Further investigation into the molecular intricacies of QSYQ's regulation of pyroptosis following myocardial infarction is warranted. This research was therefore designed to discern the process by which the active agent in QSYQ functions.
The active constituents and common target genes of QSYQ, which intervene pyroptosis following myocardial infarction, were identified by integrating network pharmacology and molecular docking strategies. Thereafter, STRING and Cytoscape were employed to build a protein-protein interaction network, enabling the identification of potential active compounds. VX-770 Using molecular docking, the binding capacity of candidate compounds to pyroptosis proteins was determined. The protective effects and mechanisms of the candidate drug were assessed in oxygen-glucose deprivation (OGD) cardiomyocyte injury models.
Two candidates with drug-like properties were initially selected, and subsequent testing verified hydrogen bonding as the mechanism of binding between Ginsenoside Rh2 (Rh2) and the primary target High Mobility Group Box 1 (HMGB1). By mitigating OGD-induced H9c2 cell demise, 2M Rh2 demonstrably reduced inflammatory cytokines IL-18 and IL-1, possibly by quelling NLRP3 inflammasome activation, hindering p12-caspase-1 expression, and decreasing the amount of pyroptosis-related GSDMD-N.