Transplanting network pharmacology technology into food science research: A comprehensive review on uncovering food-sourced functional factors and their health benefits.

Network pharmacology is an emerging interdisciplinary research method. The application of network pharmacology to reveal the nutritional effects and mechanisms of active ingredients in food is of great significance in promoting the development of functional food, facilitating personalized nutrition, and exploring the mechanisms of food health effects. This article systematically reviews the application of network pharmacology in the field of food science using a literature review method. The application progress of network pharmacology in food science is discussed, and the mechanisms of functional factors in food on the basis of network pharmacology are explored. Additionally, the limitations and challenges of network pharmacology are discussed, and future directions and application prospects are proposed. Network pharmacology serves as an important tool to reveal the mechanisms of action and health benefits of functional factors in food. It helps to conduct in-depth research on the biological activities of individual ingredients, composite foods, and compounds in food, and assessment of the potential health effects of food components. Moreover, it can help to control and enhance their functionality through relevant information during the production and processing of samples to guarantee food safety. The application of network pharmacology in exploring the mechanisms of functional factors in food is further analyzed and summarized. Combining machine learning, artificial intelligence, clinical experiments, and in vitro validation, the achievement transformation of functional factor in food driven by network pharmacology is of great significance for the future development of network pharmacology research.

The predictive value of mBDNF for major adverse cardiovascular events in stable coronary artery disease patients with depressive symptoms: A single-center, 5-year follow-up study.

BACKGROUND: Myokines play vital roles in both stable coronary artery disease (SCAD) and depression. Meanwhile, there is a pressing necessity to find effective biomarkers for early predictor of major adverse cardiovascular events (MACE) in SCAD patients with depressive symptoms. METHODS: A single-center, 5-year follow-up study was investigated. MACE was defined as composite end points, including cardiovascular death, non-fatal stroke, non-fatal myocardial infarction, coronary artery revascularization, or hospitalization for unstable angina. RESULTS: A total of 116 SCAD patients were enrolled, consisting of 30 cases (25.9%) without depressive symptoms and 86 cases (74.1%) with depressive symptoms. During the follow-up, 3 patients (2.6%) were lost. Out of 113 patients, 51 (45.1%) experienced MACE. In the subgroup of 84 SCAD patients with depressive symptoms, 44 cases (52.4%) of MACE were observed. Finally, mature brain-derived neurotrophic factor (mBDNF), pro-brain-derived neurotrophic factor, receptor activator of nuclear factor-κB ligand, smoking history, hypertension and cystatin C were incorporated into the predictive model. CONCLUSIONS: Depressive symptoms represent an independent risk factor for MACE in patients with SCAD. Additionally, low mBDNF expression may be an important early predictor for MACE in SCAD patients with depressive symptoms. The predictive model may exhibit a commendable predictive performance for MACE in SCAD patients with depressive symptoms.

Review of the epidemiology, pathogenesis and prevention of atrial fibrillation after pacemaker implantation.

Cardiac pacemaker implantation is an important treatment for symptomatic bradycardia. However, epidemiological data show that the incidence of atrial fibrillation (AF) is significantly higher in patients with implanted pacemakers than in the general population, which may be related to the preoperative presence of multiple risk factors for AF, improvement of diagnostic sensitivity and the pacemaker itself. The pathogenesis of AF after the implantation of pacemaker is related to cardiac electrical remodeling, structural remodeling, inflammation, and autonomic nervous disorder, which are induced by the pacemaker. Moreover, different pacing modes and pacing sites have various effects on the pathogenesis of postoperative AF. Recent studies have reported that reducing the proportion of ventricular pacing, improving the pacing site and setting up special pacing procedures might be highly useful in prevention of AF after pacemaker implantation. This article reviews the epidemiology, pathogenesis, influencing factors, and preventive measures regarding AF after pacemaker surgery.

The Role of Short-Chain Fatty Acids of Gut Microbiota Origin in Hypertension.

Hypertension is a significant risk factor for cardiovascular and cerebrovascular diseases, and its development involves multiple mechanisms. Gut microbiota has been reported to be closely linked to hypertension. Short-chain fatty acids (SCFAs)-the metabolites of gut microbiota-participate in hypertension development through various pathways, including specific receptors, immune system, autonomic nervous system, metabolic regulation and gene transcription. This article reviews the possible mechanisms of SCFAs in regulating blood pressure and the prospects of SCFAs as a target to prevent and treat hypertension.

New Insights Into the Comorbidity of Coronary Heart Disease and Depression.

Coronary heart disease (CHD) and depression are common disorders that markedly impair quality of life and impose a great financial burden on society. They are also frequently comorbid, exacerbating patient condition, and worsening prognosis. This comorbidity strongly suggests shared pathologic mechanisms. This review focuses on the incidence of depression in patients with CHD, deleterious effects of depression on CHD symptoms, and the potential mechanisms underlying comorbidity. In addition to the existing frequent mechanisms that are well known for decades, this review summarized interesting and original potential mechanisms to underlie the comorbidity, such as endocrine substances, gut microbiome, and microRNA. Finally, there are several treatment strategies for the comorbidity, involving drugs and psychotherapy, which may provide a theoretical basis for further basic research and clinical investigations on improved therapeutic interventions.

Deleterious effects of viral pneumonia on cardiovascular system.

Viral pneumonia has a significant effect on the cardiovascular system through various mechanisms; even though it is traditionally regarded as a pulmonary disease characterized by dyspnoea and hypoxaemia. Recent research works have shown that cardiovascular events outweigh all other causes of death in various influenza pandemics. Therefore, the exploration of the effects of viral pneumonia on cardiovascular system becomes increasingly essential. The objective of this review is three-fold: first, to summarize the knowledge about the epidemiological characteristics and clinical manifestations of viral infections that are the recent causes of global pandemics; second, to explore the cardiovascular response to these infections; and third, to attempt in identifying the possible coping strategies of the Wuhan epidemic and the future viral infection pandemics.

Nervous system involvement after infection with COVID-19 and other coronaviruses.

Viral infections have detrimental impacts on neurological functions, and even to cause severe neurological damage. Very recently, coronaviruses (CoV), especially severe acute respiratory syndrome CoV 2 (SARS-CoV-2), exhibit neurotropic properties and may also cause neurological diseases. It is reported that CoV can be found in the brain or cerebrospinal fluid. The pathobiology of these neuroinvasive viruses is still incompletely known, and it is therefore important to explore the impact of CoV infections on the nervous system. Here, we review the research into neurological complications in CoV infections and the possible mechanisms of damage to the nervous system.

Serum Levels of FGF21, ß-Klotho, and BDNF in Stable Coronary Artery Disease Patients With Depressive Symptoms: A Cross-Sectional Single-Center Study.

Background: The incidence of depressive symptoms (DS) in patients with stable coronary artery disease (SCAD) is significantly higher than those in healthy population, and that DS are independent risk factors for cardiovascular events. Previous studies have reported that fibroblast growth factor 21 (FGF21), ß-klotho, mature brain-derived neurotrophic factor (mBDNF), and BDNF precursor (proBDNF) play important roles in the pathogenesis and treatment of coronary heart disease and depression. With this in mind, the present study aimed to clarify the relationship between FGF21, ß-klotho, mBDNF, and proBDNF and SCAD with comorbid depression, in addition to also exploring the underlying mechanisms of these disease processes. Methods: A total of 116 patients with SCAD and 45 healthy controls were recruited. Patients with SCAD were further divided into two subgroups based on the Zung Self-Rating Depression Scale (SDS), which were characterized as those with no DS (NDS) and those with DS. Baseline data were collected, and serum levels of FGF21, ß-klotho, mBDNF, and proBDNF were determined. Results: In SCAD patients, Gensini scores-denoting the degree of coronary arteriostenosis-were significantly greater in the DS group than in the NDS group. There was also a positive correlation between the Gensini scores and the SDS scores. Patients in the SCAD group demonstrated a lower serum FGF21. Serum ß-klotho, mBDNF, and mBDNF/proBDNF were also significantly lower in the DS group than in the NDS group. Furthermore, ß-klotho and mBDNF were negatively correlated with the SDS scores. Additionally, SCAD patients were divided into lower- and higher-level groups using hierarchical cluster analysis, with the results highlighting that patients in the lower mBDNF group had a higher incidence of DS. Conclusions: The depression score was positively correlated with the severity of coronary artery stenosis, and serum FGF21, ß-klotho, mBDNF, and proBDNF were closely related to the development of DS in patients with SCAD. These observations suggest FGF21, ß-klotho, mBDNF, and proBDNF as potential diagnostic and/or therapeutic targets for SCAD with co-morbid depression.

Metabolic remodeling induced by mitokines in heart failure.

The prevalence rates of heart failure (HF) are greater than 10% in individuals aged >75 years, indicating an intrinsic link between aging and HF. It has been recognized that mitochondrial dysfunction contributes to the pathology of HF. Mitokines are a type of cytokines, peptides, or signaling pathways produced or activated by the nucleus or the mitochondria through cell non-autonomous responses during cellular stress. In addition to promoting the communication between the mitochondria and the nucleus, mitokines also exert a systemic regulatory effect by circulating to distant tissues. It is noteworthy that increasing evidence has demonstrated that mitokines are capable of reducing the metabolic-related HF risk factors and are associated with HF severity. Consequently, mitokines might represent a potential therapy target for HF.

Contribution of skeletal muscular glycine to rapid antidepressant effects of ketamine in an inflammation-induced mouse model of depression.

RATIONALE: Basic and clinical studies have reported rapid and long-lasting antidepressant effects of ketamine. Although previous studies have proposed several mechanisms underlying the antidepressant effects of ketamine, these mechanisms have not been completely elucidated. OBJECTIVES: The present study evaluated the effects of systemically administered ketamine treatment in a lipopolysaccharide (LPS)-induced mouse model of depression. METHODS: Non-targeted metabolomics, western blotting, and behavioral tests (locomotion, tail suspension, and forced swimming tests) were performed. RESULT: Ketamine significantly attenuated the abnormally increased immobility time in a lipopolysaccharide (LPS)-induced mouse model of depression. Aminomalonic acid, glutaraldehyde, glycine, histidine, N-methyl-L-glutamic acid, and ribose levels in skeletal muscle were altered following ketamine administration. Furthermore, ketamine significantly decreased the LPS-induced increase in glycine receptor A1 (GlyA1) levels. However, the glycine receptor antagonist strychnine did not elicit any pharmacological effects on ketamine-induced alterations in behaviors or muscular GlyA1 levels. Exogenous glycine and L-serine significantly improved depression-like symptoms in LPS-induced mice. CONCLUSIONS: Our findings suggest that skeletal muscular glycine contributes to the antidepressant effects of ketamine in inflammation. Effective strategies for improving skeletal muscular glycine levels may be a novel approach to depression treatment.

Prevalence and predisposing factors of depressive symptoms in patients with stable coronary artery disease: a cross-sectional single-center study.

The incidence of depressive symptoms in patients with stable coronary artery disease (SCAD) has significantly increased. However, its pathogenesis and treatment mechanisms are still incompletely understood. In this study, 144 patients with SCAD were recruited. Depressive symptoms of patients with SCAD were evaluated using Zung Self-Rating Depression Scale during hospitalization, and the patients were categorized into two subgroups: the non-depressive and depressive groups (further divided into mild and moderate/severe depressive groups). The rate of moderate/severe depressive symptoms in patients with SCAD was 18.8%. The mean age of patients in the depressive and mild depressive groups was older than that of those in the non-depressive group, and patients in the moderate/severe depressive group had higher high-density lipoprotein (HDL) and lower creatinine (Cr) levels. Binary logistic regression analysis showed that lower low-density lipoprotein (LDL) levels were significantly associated with increased risks of mild depressive symptoms, whereas higher HDL and lower Cr levels were significantly associated with moderate/severe depressive symptoms, suggesting that patients with SCAD were prone to experience depressive symptoms, especially in the elderly. Abnormality in LDL, HDL, and Cr levels might contribute to the depressive symptoms.

Sulforaphane Alleviates Lipopolysaccharide-induced Spatial Learning and Memory Dysfunction in Mice: The Role of BDNF-mTOR Signaling Pathway.

Peripheral immune activation could cause neuroinflammation, leading to a series of central nervous system (CNS) disorders, such as spatial learning and memory dysfunction. However, its pathogenic mechanism and therapeutic strategies are not yet determined. The present study aimed to investigate the therapeutic effects of sulforaphane (SFN) on lipopolysaccharide (LPS)-induced spatial learning and memory dysfunction, and tried to elucidate its relationship with the role of hippocampal brain-derived neurotrophic factor (BDNF)-mammalian target of rapamycin (mTOR) signaling pathway. Intraperitoneal injection of LPS for consecutive 7 days to mice caused abnormal behaviors in Morris water maze test (MWMT), while systemic administration of SFN notably reversed the abnormal behaviors. In addition, hippocampal levels of inflammatory cytokines, synaptic proteins, BDNF-tropomyosin receptor kinase B (TrkB) and mTOR signaling pathways were altered in the processes of LPS-induced cognitive dysfunction and SFN's therapeutic effects. Furthermore, we found that ANA-12 (a TrkB inhibitor) or rapamycin (a mTOR inhibitor) could block the beneficial effects of SFN on LPS-induced cognitive dysfunction, and that hippocampal levels of synaptic proteins, BDNF-TrkB and mTOR signaling pathways were also notably changed. In conclusion, the results of the present study suggest that SFN could elicit improving effects on LPS-induced spatial learning and memory dysfunction, which is likely related to the regulation of hippocampal BDNF-mTOR signaling pathway.

The Role of Cardiokines in Heart Diseases: Beneficial or Detrimental?

Cardiovascular disease remains the leading cause of morbidity and mortality, imposing a major disease burden worldwide. Therefore, there is an urgent need to identify new therapeutic targets. Recently, the concept that the heart acts as a secretory organ has attracted increasing attention. Proteins secreted by the heart are called cardiokines, and they play a critical physiological role in maintaining heart homeostasis or responding to myocardial damage and thereby influence the development of heart diseases. Given the critical role of cardiokines in heart disease, they might represent a promising therapeutic target. This review will focus on several cardiokines and discuss their roles in the pathogenesis of heart diseases and as potential therapeutics.