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Effects of curcumin on non-alcoholic fatty liver disease: A scientific metrogy study.
Li, X, Chen, W, Ren, J, Gao, X, Zhao, Y, Song, T, Fu, K, Zheng, Y, Yang, J
Phytomedicine : international journal of phytotherapy and phytopharmacology. 2024;:155241
Abstract
BACKGROUND Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases encountered in clinical practice. Curcumin can alleviate insulin resistance, inhibit oxidative stress response, reduce inflammation, reduce liver fat deposition, and effectively improve NAFLD through various modalities, inhibiting the progression into cirrhosis and fibrosis. PURPOSE To explore the current status, hot spots, and developing trends of curcumin in NAFLD treatment through quantitative scientific analysis to serve as a reference for subsequent studies. STUDY DESIGN A comprehensive analysis of the mechanism of action of curcumin in the treatment of NAFLD and methods to increase curcumin bioavailability using bibliometric analysis and literature review. METHODS This study used VOSviewer software to analyze the literature related to curcumin treatment of NAFLD in the Web of Science (WOS) core set database. A comprehensive and in-depth review was conducted based on the results of scientific econometric research and literature review. RESULTS The review observed that curcumin can activate various signaling pathways such as AMPK and NF-κB to inhibit oxidative stress and apoptosis, thereby reflecting its pharmacological effects: lowering lipid, anti-inflammatory, reducing insulin resistance, and anti-fibrosis. These mechanisms improve or even reverse the complex pathological features of lipid metabolism disorders associated with NAFLD. Curcumin also can potentially serve as a primary regulatory target for treating hepatic steatosis using gut microbiota. However, these pharmacological effects of curcumin were limited owing to its low bioavailability. CONCLUSION This review discusses NAFLD treatment with curcumin, analyzes the reasons for its low bioavailability, and introduces models for studying and methods for improving curcumin bioavailability. As research on NAFLD grows, future research should capture the trend of basic research, pay attention to clinical research, and continuously explore the therapeutic potential of curcumin.
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From bacteria to biomedicine: Developing therapies exploiting NAD+ metabolism.
Chen, Y, Ying, Y, Lalsiamthara, J, Zhao, Y, Imani, S, Li, X, Liu, S, Wang, Q
Bioorganic chemistry. 2024;:106974
Abstract
Nicotinamide adenine dinucleotide (NAD+) serves as a critical cofactor in cellular metabolism and redox reactions. Bacterial pathways rely on NAD+ participation, where its stability and concentration govern essential homeostasis and functions. This review delves into the role and metabolic regulation of NAD+ in bacteria, highlighting its influence on physiology and virulence. Notably, we explore enzymes linked to NAD+ metabolism as antibacterial drug targets and vaccine candidates. Moreover, we scrutinize NAD+'s medical potential, offering insights for its application in biomedicine. This comprehensive assessment informs future research directions in the dynamic realm of NAD+ and its biomedical significance.
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Novel HPD mutation p.A244V compound with p.T219M causing tyrosinemia type III in a Chinese girl and review of the genotype-phenotype spectrum.
Han, D, Wang, L, Zhao, C, Li, J, Huang, C, Song, W, Wang, H, Li, X, Tao, Y
Molecular genetics & genomic medicine. 2024;(1):e2298
Abstract
BACKGROUND Hereditary tyrosinemia type III (HT III) is an extremely rare form of tyrosinemia, characterized by autosomal recessive inheritance and biallelic mutations in the HPD gene. The clinical presentation of HT III is variable and poorly understood, with symptoms ranging from developmental delay and intellectual impairment to seizures and intermittent ataxia. This study aimed to provide further insights into the clinical and genetic characteristics of HT III. METHODS A 3-year-old girl, identified through newborn screening, was diagnosed with HT III using targeted next-generation sequencing. A comprehensive literature review was conducted, and the clinical, biochemical, and genetic findings of previously reported HT III patients were summarized and analyzed. RESULTS The genetic analysis of the proband revealed compound heterozygous mutations in the HPD gene such as c.731C>T (p.A244V) and c.656C>T (p.T219M). Notably, the HPD p.A244V mutation had not been previously documented in public databases or the scientific literature. Bioinformatics analysis classified both variants as pathogenic variants. The patient exhibited persistent tyrosinemia, elevated levels of related metabolite derivatives, confirming the diagnosis of HT III. The review of previously published cases contributed to a better understanding of the clinical and genetic characteristics associated with HT III. CONCLUSION Early diagnosis and prompt treatment in infancy are crucial for managing HT III effectively. Dietary therapy, particularly during childhood, plays a significant role in disease management. The findings from this study enhance our understanding of the genotype-phenotype associations in HT III and emphasize the importance of early intervention for improved patient outcomes.
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A New Perspective in the Treatment of Ischemic Stroke: Ferroptosis.
Zhang, L, Bai, XY, Sun, KY, Li, X, Zhang, ZQ, Liu, YD, Xiang, Y, Liu, XL
Neurochemical research. 2024;(4):815-833
Abstract
Ischemic stroke is a common neurological disease. Currently, there are no Food and Drug Administration-approved drugs that can maximize the improvement in ischemic stroke-induced nerve damage. Hence, treating ischemic stroke remains a clinical challenge. Ferroptosis has been increasingly studied in recent years, and it is closely related to the pathophysiological process of ischemic stroke. Iron overload, reactive oxygen species accumulation, lipid peroxidation, and glutamate accumulation associated with ferroptosis are all present in ischemic stroke. This article focuses on describing the relationship between ferroptosis and ischemic stroke and summarizes the relevant substances that ameliorate ischemic stroke-induced neurological damage by inhibiting ferroptosis. Finally, the problems in the treatment of ischemic stroke targeting ferroptosis are discussed, hoping to provide a new direction for its treatment.
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Amino acid metabolism, redox balance and epigenetic regulation in cancer.
Li, X, Zhang, HS
The FEBS journal. 2024;(3):412-429
Abstract
Amino acids act as versatile nutrients driving cell growth and survival, especially in cancer cells. Amino acid metabolism comprises numerous metabolic networks and is closely linked with intracellular redox balance and epigenetic regulation. Reprogrammed amino acid metabolism has been recognized as a ubiquitous feature in tumour cells. This review outlines the metabolism of several primary amino acids in cancer cells and highlights the pivotal role of amino acid metabolism in sustaining redox homeostasis and regulating epigenetic modification in response to oxidative and genetic stress in cancer cells.
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Therapeutics for neurodegenerative diseases by targeting the gut microbiome: from bench to bedside.
Ma, YY, Li, X, Yu, JT, Wang, YJ
Translational neurodegeneration. 2024;(1):12
Abstract
The aetiologies and origins of neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD), are complex and multifaceted. A growing body of evidence suggests that the gut microbiome plays crucial roles in the development and progression of neurodegenerative diseases. Clinicians have come to realize that therapeutics targeting the gut microbiome have the potential to halt the progression of neurodegenerative diseases. This narrative review examines the alterations in the gut microbiome in AD, PD, ALS and HD, highlighting the close relationship between the gut microbiome and the brain in neurodegenerative diseases. Processes that mediate the gut microbiome-brain communication in neurodegenerative diseases, including the immunological, vagus nerve and circulatory pathways, are evaluated. Furthermore, we summarize potential therapeutics for neurodegenerative diseases that modify the gut microbiome and its metabolites, including diets, probiotics and prebiotics, microbial metabolites, antibacterials and faecal microbiome transplantation. Finally, current challenges and future directions are discussed.
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Dietary Fibre for the Prevention of Post-Pancreatitis Diabetes Mellitus: A Review of the Literature and Future Research Directions.
Li, X, Petrov, MS
Nutrients. 2024;(3)
Abstract
Post-pancreatitis diabetes mellitus-the most common sequela of pancreatitis-leads to poorer glycaemic control compared with type 2 diabetes. Because post-pancreatitis diabetes mellitus is an exemplar of secondary diabetes (with a clear underlying cause), much post-pancreatitis diabetes mellitus is preventable or treatable early. Earlier literature established the important role of dietary fibre in reducing plasma glucose in individuals with type 2 diabetes. The present review benchmarks available evidence on the role of habitual dietary fibre intake in pancreatitis and post-pancreatitis diabetes mellitus. It also paves the way for future research on the use of dietary fibre in the post-pancreatitis setting.
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Prognostic potential of nutritional risk screening and assessment tools in predicting survival of patients with pancreatic neoplasms: a systematic review.
Yu, M, Li, X, Chen, M, Liu, L, Yao, T, Li, J, Su, W
Nutrition journal. 2024;(1):17
Abstract
BACKGROUNDS & AIMS The nutritional evaluation of pancreatic cancer (PC) patients lacks a gold standard or scientific consensus, we aimed to summarize and systematically evaluate the prognostic value of nutritional screening and assessment tools used for PC patients. METHODS Relevant studies were retrieved from major databases (PubMed, Embase, Web of Science, Cochrane Library) and searched from January 2010 to December 2023. We performed meta-analyses with STATA 14.0 when three or more studies used the same tool. RESULTS This analysis included 27 articles involving 6,060 PC patients. According to a meta-analysis of these studies, poor nutritional status evaluated using five nutritional screening tools Prognostic Nutritional Index (PNI), Geriatric Nutritional Risk Index (GNRI), Controlling Nutritional Status Score (CONUT), Nutrition Risk Screening (NRS2002) and Glasgow Prognostic Score (GPS) was associated with all-cause mortality in PC patients. But Modified Glasgow Prognostic Score (mGPS) did not. Of all tools analyzed, CONUT had the maximum HR for mortality (HR = 1.978, 95%CI 1.345-2.907, P = 0.001). CONCLUSION All-cause mortality in PC patients was predicted by poor nutritional status. CONUT may be the best nutritional assessment tool for PC patients. The clinical application value of Short Form Mini Nutritional Assessment (MNA-SF), Generated Subjective Global Assessment (SGA) and Patient-generated Subjective Global Assessment (PG-SGA) in PC patients need to be confirmed. In order to improve patients' nutritional status and promote their recovery, nutritional screening tools can be used. REGISTRATION This systematic review was registered at the International Prospective Register of Systematic Reviews (PROSPERO) (number CRD42022376715).
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The potential role of glucose metabolism, lipid metabolism, and amino acid metabolism in the treatment of Parkinson's disease.
Li, H, Zeng, F, Huang, C, Pu, Q, Thomas, ER, Chen, Y, Li, X
CNS neuroscience & therapeutics. 2024;(2):e14411
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Abstract
PURPOSE OF REVIEW Parkinson's disease (PD) is a common neurodegenerative disease, which can cause progressive deterioration of motor function causing muscle stiffness, tremor, and bradykinesia. In this review, we hope to describe approaches that can improve the life of PD patients through modifications of energy metabolism. RECENT FINDINGS The main pathological features of PD are the progressive loss of nigrostriatal dopaminergic neurons and the production of Lewy bodies. Abnormal aggregation of α-synuclein (α-Syn) leading to the formation of Lewy bodies is closely associated with neuronal dysfunction and degeneration. The main causes of PD are said to be mitochondrial damage, oxidative stress, inflammation, and abnormal protein aggregation. Presence of abnormal energy metabolism is another cause of PD. Many studies have found significant differences between neurodegenerative diseases and metabolic decompensation, which has become a biological hallmark of neurodegenerative diseases. SUMMARY In this review, we highlight the relationship between abnormal energy metabolism (Glucose metabolism, lipid metabolism, and amino acid metabolism) and PD. Improvement of key molecules in glucose metabolism, fat metabolism, and amino acid metabolism (e.g., glucose-6-phosphate dehydrogenase, triglycerides, and levodopa) might be potentially beneficial in PD. Some of these metabolic indicators may serve well during the diagnosis of PD. In addition, modulation of these metabolic pathways may be a potential target for the treatment and prevention of PD.
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SLC40A1 in iron metabolism, ferroptosis, and disease: A review.
Zhang, Y, Zou, L, Li, X, Guo, L, Hu, B, Ye, H, Liu, Y
WIREs mechanisms of disease. 2024;:e1644
Abstract
Solute carrier family 40 member 1 (SLC40A1) plays an essential role in transporting iron from intracellular to extracellular environments. When SLC40A1 expression is abnormal, cellular iron metabolism becomes dysregulated, resulting in an overload of intracellular iron, which induces cell ferroptosis. Numerous studies have confirmed that ferroptosis is closely associated with the development of many diseases. Here, we review recent findings on SLC40A1 in ferroptosis and its association with various diseases, intending to explore new directions for research on disease pathogenesis and new therapeutic targets for prevention and treatment. This article is categorized under: Cancer > Genetics/Genomics/Epigenetics Metabolic Diseases > Molecular and Cellular Physiology.