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• Protein-protein interaction network analysis identified six pivotal proteins (TNF, IL6, TLR4, IL1β, IL10, IL8) with the potential as targets. • miRNAs regulating the identified target genes may also be important regulators of malaria susceptibility. • Host genetics plays a significant role in malaria susceptibility.. Malaria is a deadly blood-borne disease caused by a Plasmodium parasite. Infection results in various forms of malaria, including an asymptomatic state, uncomplicated disease, or severe disease. Severe malaria (SM) is particularly prevalent among young children and is a significant cause of mortality. SM is associated with the sequestration of parasitized erythrocytes in the microvasculature of vital host organs, disrupting the normal functioning of the immune system. Although the exact mechanisms of malaria pathogenesis are yet to be fully understood, researchers have been investigating the role of host genetics in determining the severity of the disease and the outcome of infection. The objective of this study is to identify specific host genes that have been examined for their association with malaria in Asian populations and pinpoint those most likely to influence susceptibility. Through an extensive screening process, a total of 982 articles were initially identified, and after careful review, 40 articles discussing 68 genes were included in this review. By constructing a network of protein-protein interactions (PPIs), we identified six key proteins (TNF, IL6, TLR4, IL1β, IL10, and IL8) that exhibited substantial interactions (more than 30 edges), suggesting their potential as significant targets for influencing malaria susceptibility. Notably, these six proteins have been previously identified as crucial components of the immune response, associated with malaria susceptibility, and capable of affecting different clinical forms of the disease. Identifying genes that contribute to malaria susceptibility or resistance holds the promise of enhancing the diagnosis and treatment of this debilitating illness. Such knowledge has the potential to pave the way for more targeted and effective strategies in combating malaria, particularly in Asian populations where controlling Plasmodium vivax is challenging, and India contributes the highest number of cases. By understanding the genetic factors underlying malaria vulnerability, we can develop interventions that are tailored to the specific needs of Asian populations, ultimately leading to better outcomes in the fight against this disease. [ABSTRACT FROM AUTHOR]

Follicular lymphoma (FL) is the most common indolent B-cell lymphoma (BCL) globally. Recently, its incidence has increased in Europe, the United States, and Asia, with the number of gastrointestinal FL cases expected to increase. Genetic abnormalities related to t(14;18) translocation, BCL2 overexpression, NF-κB pathway-related factors, histone acetylases, and histone methyltransferases cause FL and enhance its proliferation. Meanwhile, microRNAs are commonly used in diagnosing FL and predicting patient prognosis. Many clinical trials on novel therapeutics targeting these genetic abnormalities and immunomodulatory mechanisms have been conducted, resulting in a marked improvement in therapeutic outcomes for FL. Although developing these innovative therapeutic agents targeting specific genetic mutations and immune pathways has provided hope for curative options, FL treatment has become more complex, requiring combinatorial therapeutic regimens. However, optimal treatment combinations have not yet been achieved, highlighting the importance of a complete under-standing regarding the pathogenesis of gastrointestinal FL. Accordingly, this article reviews key research on the molecular pathogenesis of nodal FL and novel therapies targeting the causative genetic mutations. Moreover, the results of clinical trials are summarized, with a particular focus on treating nodal and gastrointestinal FLs., Competing Interests: Conflict-of-interest statement: There is no conflict of interest to disclose., (©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.)

Esophageal cancer is one of the leading causes of cancer death in the male population of Eastern Asia. In addition, esophageal squamous cell carcinoma (ESCC) is the major type of esophageal cancer among the world. Owing to the poor overall 5-year survival rate, novel effective treatment strategies are needed. MicroRNAs are important gene regulators that are dysregulated in many cancer types. In our previous study, we applied next-generation sequencing to demonstrate that miR-338-5p was downregulated in the tumor tissue of patients with versus without recurrence. In this study, we further studied the roles of miR-338-5p in ESCC. The expression of endogenous miR-338-5p was at lower levels in ESCC cells compared with normal cells. Functional assays showed that miR-338-5p reduced cell proliferation, colony formation, migration and cisplatin resistance in an ESCC cell line, CE-81T. Potential target genes of miR-338-5p were identified by microarray and prediction tools, and 31 genes were selected. Among these, Fermitin family homolog 2 (FERMT2) plays an oncogenic role in ESCC, so it was chosen for further study. Luciferase assays showed the direct binding between miR-338-5p and the 3′ untranslated region of FERMT2. Silencing of FERMT2 inhibited cell proliferation, colony formation, migration and cisplatin resistance. Pathway analysis revealed that the integrin-linked protein kinase signaling pathway, in which FERMT2 participates, was significantly affected by a miR-338-5p mimic. Our results suggest that miR-338-5p may play an antioncogenic role in ESCC via repressing FERMT2. [ABSTRACT FROM AUTHOR]

• Geniposide ameliorates hepatocyte fatty degeneration and increases plaque stability. • Geniposide regulates the expression of certain miRNAs in inflammation. • Geniposide increases the protein expression of MKP-1, a target of miR-101, in ApoE−/− mice and Raw264.7 cells induced by LPS. • Geniposide downregulates the transcriptional level of miR-101 and suppresses the levels of inflammatory factors in the presence of the miR-101 mimic. Atherosclerosis (AS) is the common pathological basis of chronic cardiovascular diseases and is associated with inflammation and lipid metabolism dysfunction. Geniposide, the main active ingredient of Gardenia jasminoides Ellis fruit, exhibits a variety of anti-inflammatory and anti-oxidative functions; however, its role in AS remains unclear. The aim of this study was to investigate the mechanisms of geniposide in alleviating inflammation and thereby attenuating the development of AS. ApoE−/− mice were fed a high fat diet to induce AS and were treated with geniposide (50 mg/kg) for 12 weeks. Blood glucose and lipid levels were measured by biochemical analysis. H&E, Masson and Oil red O staining were performed to observe morphological changes and lipid deposition in the aorta and liver. Serum inflammatory cytokines were detected by ELISA. Dual-luciferase reporter gene assay was used to verify the target relationship between microRNA-101 (miR-101) and mitogen-activated protein kinase phosphatase-1 (MKP-1). The levels of miR-101, p-p38, and MKP-1 in the aorta were detected by q PCR and western blotting. The anti-inflammatory effect of geniposide in vitro was investigated in the RAW264.7 macrophage cell line. A miR-101 mimic and an inhibitor were used to study the effect of miR-101 on regulating the expression of the target MKP-1 and the downstream inflammatory cytokines. Geniposide treatment reduced lipid levels and plaque size in the mouse model of AS. Geniposide downregulated miR-101 to upregulate MKP-1 and suppress the production of inflammatory factors in vitro and in vivo. Geniposide suppressed the levels of inflammatory factors in the presence of the miR-101 mimic, whereas no obvious effect was observed in the miR-101 inhibitor group. We concluded that geniposide reduced the plaque size and alleviated inflammatory injury in ApoE−/− mice and RAW264.7 cells. The specific anti-inflammatory mechanism was related to the miR-101/ MKP-1/p38 signaling pathway. [ABSTRACT FROM AUTHOR]

• Differentially expressed miRNAs were obtained from CIV-infected primary CBECs, CAMCs. • Two miRNA expressions were significantly decreased in canine infected primary cells. • Overexpressed of the two miRNAs inhibited H3N2 CIV infection. • Cfa-miR-125b and cfa-miR-151 acted as negative regulators in H3N2 CIV infection. MicroRNAs (miRNAs) are known to play important regulatory roles in host-virus interactions. Avian-origin H3N2 canine influenza virus (CIV) has emerged as the most prevalent subtype among dogs in Asia since 2007. To evaluate the roles of host miRNAs in H3N2 CIV infection, here, miRNA profiles obtained from primary canine bronchiolar epithelial cells (CBECs) and canine alveolar macrophages (CAMCs) were compared between infected and mock-infected cells with the H3N2 CIV JS/10. It was found that the expressions of cfa-miR-125b and cfa-miR-151, which have been reported to be associated with innate immunity and inflammatory response, were significantly decreased in CIV-infected canine primary cells. Bioinformatics prediction indicated that 5′ seed regions of the two miRNAs are partially complementary to the mRNAs of nucleoprotein (NP) and non-structural protein 1 (NS1) of JS/10. As determined by virus titration, quantitative real-time PCR (qRT-PCR) and western blotting, overexpression of the two miRNAs inhibited CIV replication in cell culture, while their inhibition facilitated this replication, suggesting that the two miRNAs could act as negative regulators of CIV replication. Our findings support the notion that some cellular miRNAs can influence the outcome of virus infection, which helps to elucidate the resistance of host cells to viral infection and to clarify the pathogenesis of H3N2 CIV. [ABSTRACT FROM AUTHOR]

Background Because of a nonresponse to aspirin (aspirin resistance), patients with acute coronary syndrome (ACS) are at increased risk of developing recurrent event. The in vitro platelet function tests have potential limitations, making them unsuitable for the detection of aspirin resistance. We investigated whether miR-19b-1-5p could be utilized as a biomarker for aspirin resistance and future major adverse cardio-cerebrovascular (MACCE) events in patients with ACS. Methods and Results In this cohort study, patients with ACS were enrolled from multiple tertiary hospitals in Christchurch, Hong Kong, Sarawak, and Singapore between 2011 and 2015. MiR-19b-1-5p expression was measured from buffy coat of patients with ACS (n=945) by reverse transcription quantitative polymerase chain reaction. Platelet function was determined by Multiplate aggregometry testing. MACCE was collected over a mean follow-up time of 1.01±0.43 years. Low miR-19b-1-5p expression was found to be related to aspirin resistance as could be observed from sustained platelet aggregation in the presence of aspirin (-Log-miR-19b-1-5p, [unstandardized beta, 44.50; 95% CI, 2.20-86.80; P <0.05]), even after adjusting for age, sex, ethnicity, and prior history of stroke. Lower miR-19b-1-5p expression was independently associated with a higher risk of MACCE (-Log-miR-19b-1-5p, [hazard ratio, 1.85; 95% CI, 1.23-2.80; P <0.05]). Furthermore, a significant interaction was noted between the inverse miR-19b-1-5p expression and family history of premature coronary artery disease ( P =0.01) on the risk of MACCE. Conclusions Lower miR-19b-1-5p expression was found to be associated with sustained platelet aggregation on aspirin, and a higher risk of MACCE in patients with ACS. Therefore, miR-19b-1-5p could be a suitable marker for aspirin resistance and might predict recurrence of MACCE in patients with ACS.