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1.
Role of ferroptosis in chronic kidney disease.
Li, S, Han, Q, Liu, C, Wang, Y, Liu, F, Pan, S, Zuo, L, Gao, D, Chen, K, Feng, Q, et al
Cell communication and signaling : CCS. 2024;(1):113
Abstract
Chronic kidney disease (CKD) has historically been a significant global health concern, profoundly impacting both life and well-being. In the process of CKD, with the gradual loss of renal function, the incidence of various life-threatening complications, such as cardiovascular diseases, cerebrovascular accident, infection and stroke, is also increasing rapidly. Unfortunately, existing treatments exhibit limited ability to halt the progression of kidney injury in CKD, emphasizing the urgent need to delve into the precise molecular mechanisms governing the occurrence and development of CKD while identifying novel therapeutic targets. Renal fibrosis, a typical pathological feature of CKD, plays a pivotal role in disrupting normal renal structures and the loss of renal function. Ferroptosis is a recently discovered iron-dependent form of cell death characterized by lipid peroxide accumulation. Ferroptosis has emerged as a potential key player in various diseases and the initiation of organ fibrosis. Substantial evidence suggests that ferroptosis may significantly contribute to the intricate interplay between CKD and its progression. This review comprehensively outlines the intricate relationship between CKD and ferroptosis in terms of iron metabolism and lipid peroxidation, and discusses the current landscape of pharmacological research on ferroptosis, shedding light on promising avenues for intervention. It further illustrates recent breakthroughs in ferroptosis-related regulatory mechanisms implicated in the progression of CKD, thereby providing new insights for CKD treatment. Video Abstract.
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From hyperglycemia to intervertebral disc damage: exploring diabetic-induced disc degeneration.
Li, S, Du, J, Huang, Y, Gao, S, Zhao, Z, Chang, Z, Zhang, X, He, B
Frontiers in immunology. 2024;:1355503
Abstract
The incidence of lumbar disc herniation has gradually increased in recent years, and most patients have symptoms of low back pain and nerve compression, which brings a heavy burden to patients and society alike. Although the causes of disc herniation are complex, intervertebral disc degeneration (IDD) is considered to be the most common factor. The intervertebral disc (IVD) is composed of the upper and lower cartilage endplates, nucleus pulposus, and annulus fibrosus. Aging, abnormal mechanical stress load, and metabolic disorders can exacerbate the progression of IDD. Among them, high glucose and high-fat diets (HFD) can lead to fat accumulation, abnormal glucose metabolism, and inflammation, which are considered important factors affecting the homeostasis of IDD. Diabetes and advanced glycation end products (AGEs) accumulation- can lead to various adverse effects on the IVD, including cell senescence, apoptosis, pyroptosis, proliferation, and Extracellular matrix (ECM) degradation. While current research provides a fundamental basis for the treatment of high glucose-induced IDD patients. further exploration into the mechanisms of abnormal glucose metabolism affecting IDD and in the development of targeted drugs will provide the foundation for the effective treatment of these patients. We aimed to systematically review studies regarding the effects of hyperglycemia on the progress of IDD.
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Association of dietary inflammatory index and the SARS-CoV-2 infection incidence, severity and mortality of COVID-19: a systematic review and dose-response meta-analysis.
Hao, X, Li, S, Yang, Y, Dai, H, Yan, Y, Li, D
Nutrition journal. 2024;(1):21
Abstract
BACKGROUND Several studies have reported the association between dietary inflammatory index (DII) and the SARS-CoV-2 infection risk, severity or mortality of COVID-19, however, the outcomes remain controversial. OBJECTIVE We sought to examine whether a dose-response association of DII and SARS-CoV-2 infection exists. DESIGN A dose-response meta-analysis was performed to investigate the association of DII and SARS-CoV-2 infection. We conducted a systematic search of PubMed, Embase and Web of Science up to March 15th, 2023. The odds ratios (OR) of DII and COVID-19 risk and severity were computed. RESULTS Totally, 5 studies were included (1 from UK and 4 from Iran), consisting of 197,929 participants with 12,081 COVID-19 cases. Although there was heterogeneity among studies, the results indicated that higher DII was independently related to higher SARS-CoV-2 infection incidence (OR = 1.57, 95% CI: 1.14, 2.17) and COVID-19 severity (OR = 1.11, 95% CI: 1.07, 1.15) but not COVID-19 mortality (risk ratio = 1.13, 95% CI: 1.00, 1.27). The incidence of SARS-CoV-2 infection increased by 31% for each 1-point increase in the E-DII (OR = 1.31, 95% CI: 1.20, 1.43). CONCLUSIONS This meta-analysis suggests that an elevated DII score is associated with increased SARS-CoV-2 infectious risk and severity of COVID-19. There were not enough studies on COVID-19 mortality. Further large prospective studies in different countries are warranted to validate our results.
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Multiple delivery strategies of nanocarriers for myocardial ischemia-reperfusion injury: current strategies and future prospective.
Li, S, Li, F, Wang, Y, Li, W, Wu, J, Hu, X, Tang, T, Liu, X
Drug delivery. 2024;(1):2298514
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Abstract
Acute myocardial infarction, characterized by high morbidity and mortality, has now become a serious health hazard for human beings. Conventional surgical interventions to restore blood flow can rapidly relieve acute myocardial ischemia, but the ensuing myocardial ischemia-reperfusion injury (MI/RI) and subsequent heart failure have become medical challenges that researchers have been trying to overcome. The pathogenesis of MI/RI involves several mechanisms, including overproduction of reactive oxygen species, abnormal mitochondrial function, calcium overload, and other factors that induce cell death and inflammatory responses. These mechanisms have led to the exploration of antioxidant and inflammation-modulating therapies, as well as the development of myocardial protective factors and stem cell therapies. However, the short half-life, low bioavailability, and lack of targeting of these drugs that modulate these pathological mechanisms, combined with liver and spleen sequestration and continuous washout of blood flow from myocardial sites, severely compromise the expected efficacy of clinical drugs. To address these issues, employing conventional nanocarriers and integrating them with contemporary biomimetic nanocarriers, which rely on passive targeting and active targeting through precise modifications, can effectively prolong the duration of therapeutic agents within the body, enhance their bioavailability, and augment their retention at the injured myocardium. Consequently, these approaches significantly enhance therapeutic effectiveness while minimizing toxic side effects. This article reviews current drug delivery systems used for MI/RI, aiming to offer a fresh perspective on treating this disease.
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Natural products targeting the MAPK-signaling pathway in cancer: overview.
Shi, A, Liu, L, Li, S, Qi, B
Journal of cancer research and clinical oncology. 2024;(1):6
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Abstract
PURPOSE This article summarizes natural products that target the MAPK-signaling pathway in cancer therapy. The classification, chemical structures, and anti-cancer mechanisms of these natural products are elucidated, and comprehensive information is provided on their potential use in cancer therapy. METHODS Using the PubMed database, we searched for keywords, including "tumor", "cancer", "natural product", "phytochemistry", "plant chemical components", and "MAPK-signaling pathway". We also screened for compounds with well-defined structures that targeting the MAPK-signaling pathway and have anti-cancer effects. We used Kingdraw software and Adobe Photoshop software to draw the chemical compound structural diagrams. RESULTS A total of 131 papers were searched, from which 85 compounds with well-defined structures were selected. These compounds have clear mechanisms for targeting cancer treatment and are mainly related to the MAPK-signaling pathway. Examples include eupatilin, carvacrol, oridonin, sophoridine, diosgenin, and juglone. These chemical components are classified as flavonoids, phenols, terpenoids, alkaloids, steroidal saponins, and quinones. CONCLUSIONS Certain MAPK pathway inhibitors have been used for clinical treatment. However, the clinical feedback has not been promising because of genomic instability, drug resistance, and side effects. Natural products have few side effects, good medicinal efficacy, a wide range of sources, individual heterogeneity of biological activity, and are capable of treating disease from multiple targets. These characteristics make natural products promising drugs for cancer treatment.
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Mapping the Research of Ferroptosis in Parkinson's Disease from 2013 to 2023: A Scientometric Review.
Chen, Y, Wu, Z, Li, S, Chen, Q, Wang, L, Qi, X, Tian, C, Yang, M
Drug design, development and therapy. 2024;:1053-1081
Abstract
METHODS Related studies on PD and ferroptosis were searched in Web of Science Core Collection (WOSCC) from inception to 2023. VOSviewer, CiteSpace, RStudio, and Scimago Graphica were employed as bibliometric analysis tools to generate network maps about the collaborations between authors, countries, and institutions and to visualize the co-occurrence and trends of co-cited references and keywords. RESULTS A total of 160 original articles and reviews related to PD and ferroptosis were retrieved, produced by from 958 authors from 162 institutions. Devos David was the most prolific author, with 9 articles. China and the University of Melbourne had leading positions in publication volume with 84 and 12 publications, respectively. Current hot topics focus on excavating potential new targets for treating PD based on ferroptosis by gaining insight into specific molecular mechanisms, including iron metabolism disorders, lipid peroxidation, and imbalanced antioxidant regulation. Clinical studies aimed at treating PD by targeting ferroptosis remain in their preliminary stages. CONCLUSION A continued increase was shown in the literature within the related field over the past decade. The current study suggested active collaborations among authors, countries, and institutions. Research into the pathogenesis and treatment of PD based on ferroptosis has remained a prominent topic in the field in recent years, indicating that ferroptosis-targeted therapy is a potential approach to halting the progression of PD.
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Functional significance of O-linked N-acetylglucosamine protein modification in regulating autophagy.
Zhu, Z, Ren, W, Li, S, Gao, L, Zhi, K
Pharmacological research. 2024;:107120
Abstract
Autophagy is a core molecular pathway that preserves cellular and organismal homeostasis. Being susceptible to nutrient availability and stress, eukaryotic cells recycle or degrade internal components via membrane transport pathways to provide sustainable biological molecules and energy sources. The dysregulation of this highly conserved physiological process has been strongly linked to human disease. Post-translational modification, a mechanism that regulates protein function, plays a crucial role in autophagy regulation. O-linked N-acetylglucosamine protein modification (O-GlcNAcylation), a monosaccharide post-translational modification of intracellular proteins, is essential in nutritional and stress regulatory mechanisms. O-GlcNAcylation has emerged as an essential regulatory mechanism of autophagy. It regulates autophagy throughout its lifetime by targeting the core components of the autophagy regulatory network. This review provides an overview of the O-GlcNAcylation of autophagy-associated proteins and their regulation and function in the autophagy pathway. Therefore, this article may contribute to further understanding of the role of O-GlcNAc-regulated autophagy and provide new perspectives for the treatment of human diseases.
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Correlation between sarcopenia and esophageal cancer: a narrative review.
Li, S, Xie, K, Xiao, X, Xu, P, Tang, M, Li, D
World journal of surgical oncology. 2024;(1):27
Abstract
BACKGROUND In recent years, the research on the relationship between sarcopenia before and after the treatment of esophageal cancer, as well as its impact on prognosis of esophageal cancer, has increased rapidly, which has aroused people's attention to the disease of patients with esophageal cancer complicated with sarcopenia. This review examines the prevalence of sarcopenia in patients with esophageal cancer, as well as the relationship between sarcopenia (before and after surgery or chemotherapy) and prognosis in patients with esophageal cancer. Moreover, we summarized the potential pathogenesis of sarcopenia and pharmacologic and non-pharmacologic therapies. METHODS A narrative review was performed in PubMed and Web of Science using the keywords ("esophageal cancer" or "esophageal neoplasm" or "neoplasm, esophageal" or "esophagus neoplasm" or "esophagus neoplasms" or "neoplasm, esophagus" or "neoplasms, esophagus" or "neoplasms, esophageal" or "cancer of esophagus" or "cancer of the esophagus" or "esophagus cancer" or "cancer, esophagus" or "cancers, esophagus" or "esophagus cancers" or "esophageal cancer" or "cancer, esophageal" or "cancers, esophageal" or "esophageal cancers") and ("sarcopenia" or "muscular atrophy" or "aging" or "senescence" or "biological aging" or "aging, biological" or "atrophies, muscular" or "atrophy, muscular" or "muscular atrophies" or "atrophy, muscle" or "atrophies, muscle" or "muscle atrophies"). Studies reporting relationship between sarcopenia and esophageal cancer were analyzed. RESULTS The results of the review suggest that the average prevalence of sarcopenia in esophageal cancer was 46.3% ± 19.6% ranging from 14.4 to 81% and sarcopenia can be an important predictor of poor prognosis in patients with esophageal cancer. Patients with esophageal cancer can suffer from sarcopenia due to their nutritional deficiencies, reduced physical activity, chemotherapy, and the effects of certain inflammatory factors and pathways. When classic diagnostic values for sarcopenia such as skeletal muscle index (SMI) are not available clinically, it is also feasible to predict esophageal cancer prognosis using simpler metrics, such as calf circumference (CC), five-count sit-up test (5-CST), and six-minute walk distance (6MWD). CONCLUSIONS Identifying the potential mechanism of sarcopenia in patients with esophageal cancer and implementing appropriate interventions may hold the key to improving the prognosis of these patients.
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Efficacy and tolerability of FDA-approved atypical antipsychotics for the treatment of bipolar depression: a systematic review and network meta-analysis.
Li, S, Xu, C, Hu, S, Lai, J
European psychiatry : the journal of the Association of European Psychiatrists. 2024;(1):e29
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Abstract
We employed a Bayesian network meta-analysis for comparison of the efficacy and tolerability of US Food and Drug Administration (FDA)-approved atypical antipsychotics (AAPs) for the treatment of bipolar patients with depressive episodes. Sixteen randomized controlled trials with 7234 patients treated by one of the five AAPs (cariprazine, lumateperone, lurasidone, olanzapine, and quetiapine) were included. For the response rate (defined as an improvement of ≥50% from baseline on the Montgomery-Åsberg Depression Rating Scale [MADRS]), all AAPs were more efficacious than placebo. For the remission rate (defined as the endpoint of MADRS ≤12 or ≤ 10), cariprazine, lurasidone, olanzapine, and quetiapine had higher remission rates than placebo. In terms of tolerability, olanzapine was unexpectedly associated with lower odds of all-cause discontinuation in comparison with placebo, whereas quetiapine was associated with higher odds of discontinuation due to adverse events than placebo. Compared with placebo, lumateperone, olanzapine, and quetiapine showed higher odds of somnolence. Lumateperone had a lower rate of ≥ weight gain of 7% than placebo and other treatments. Olanzapine was associated with a significant increase from baseline in total cholesterol and triglycerides than placebo. These findings inform individualized prescriptions of AAPs for treating bipolar depression in clinical practice.
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Copper homeostasis in chronic kidney disease and its crosstalk with ferroptosis.
Jiayi, H, Ziyuan, T, Tianhua, X, Mingyu, Z, Yutong, M, Jingyu, W, Hongli, Z, Li, S
Pharmacological research. 2024;:107139
Abstract
Chronic kidney disease (CKD) has become a global public health problem with high morbidity and mortality. Renal fibrosis can lead to end-stage renal disease (ESRD). However, there is still no effective treatment to prevent or delay the progression of CKD into ESRD. Therefore, exploring the pathogenesis of CKD is essential for preventing and treating CKD. There are a variety of trace elements in the human body that interact with each other within a complex regulatory network. Iron and copper are both vital trace elements in the body. They are critical for maintaining bodily functions, and the dysregulation of their metabolism can cause many diseases, including kidney disease. Ferroptosis is a new form of cell death characterized by iron accumulation and lipid peroxidation. Studies have shown that ferroptosis is closely related to kidney disease. However, the role of abnormal copper metabolism in kidney disease and its relationship with ferroptosis remains unclear. Here, our current knowledge regarding copper metabolism, its regulatory mechanism, and the role of abnormal copper metabolism in kidney diseases is summarized. In addition, we discuss the relationship between abnormal copper metabolism and ferroptosis to explore the possible pathogenesis and provide a potential therapeutic target for CKD.