Pan-cancer analysis and the oncogenic role of Glypican 1 in hepatocellular carcinoma.

Recent studies indicate that Glypican 1 (GPC-1) is aberrantly expressed and plays a key role in certain cancers, but little is known in the hepatocellular carcinoma. Raw data from TCGA, GTEx and TIMER databases were utilized to comprehensively analyze GPC-1 expression landscape in pan-cancer, and the biological function of GPC-1 was investigated in liver cancer cells. The results revealed that GPC-1 is highly expressed in HCC, negatively correlated with survival, and also positively correlated with immune infiltration and clinical stage. Furthermore, GPC-1 promoted cell proliferation and inhibited apoptosis in the HCC cell lines. WGCNA analysis and HCCDB database revealed that Akt acted as a key molecule related to GPC-1, influencing biological functions and regulating cell malignant behaviors via the AKT signaling pathway. In conclusion, our findings provide a relatively comprehensive understanding of the oncogenic role of GPC-1 in HCC, implying that GPC-1 could serve as an innovative therapeutic target.

Rhodiola rosea: a review in the context of PPPM approach.

A natural "medicine and food" plant, Rhodiola rosea (RR) is primarily made up of organic acids, phenolic compounds, sterols, glycosides, vitamins, lipids, proteins, amino acids, trace elements, and other physiologically active substances. In vitro, non-clinical and clinical studies confirmed that it exerts anti-inflammatory, antioxidant, and immune regulatory effects, balances the gut microbiota, and alleviates vascular circulatory disorders. RR can prolong life and has great application potential in preventing and treating suboptimal health, non-communicable diseases, and COVID-19. This narrative review discusses the effects of RR in preventing organ damage (such as the liver, lung, heart, brain, kidneys, intestines, and blood vessels) in non-communicable diseases from the perspective of predictive, preventive, and personalised medicine (PPPM/3PM). In conclusion, as an adaptogen, RR can provide personalised health strategies to improve the quality of life and overall health status.

AURKB/CDC37 complex promotes clear cell renal cell carcinoma progression via phosphorylating MYC and constituting an AURKB/E2F1-positive feedforward loop.

As the second most common malignant tumor in the urinary system, renal cell carcinoma (RCC) is imperative to explore its early diagnostic markers and therapeutic targets. Numerous studies have shown that AURKB promotes tumor development by phosphorylating downstream substrates. However, the functional effects and regulatory mechanisms of AURKB on clear cell renal cell carcinoma (ccRCC) progression remain largely unknown. In the current study, we identified AURKB as a novel key gene in ccRCC progression based on bioinformatics analysis. Meanwhile, we observed that AURKB was highly expressed in ccRCC tissue and cell lines and knockdown AURKB in ccRCC cells inhibit cell proliferation and migration in vitro and in vivo. Identified CDC37 as a kinase molecular chaperone for AURKB, which phenocopy AURKB in ccRCC. AURKB/CDC37 complex mediate the stabilization of MYC protein by directly phosphorylating MYC at S67 and S373 to promote ccRCC development. At the same time, we demonstrated that the AURKB/CDC37 complex activates MYC to transcribe CCND1, enhances Rb phosphorylation, and promotes E2F1 release, which in turn activates AURKB transcription and forms a positive feedforward loop in ccRCC. Collectively, our study identified AURKB as a novel marker of ccRCC, revealed a new mechanism by which the AURKB/CDC37 complex promotes ccRCC by directly phosphorylating MYC to enhance its stability, and first proposed AURKB/E2F1-positive feedforward loop, highlighting AURKB may be a promising therapeutic target for ccRCC.

Variability in soybean yield responses to elevated atmospheric CO2: Insights from non-structural carbohydrate remobilisation during seed filling.

The increasing atmospheric CO2 concentration (e[CO2]) has mixed effects on soybean most varieties' yield. This study elucidated the effect of e[CO2] on soybean yield and the underlying mechanisms related to photosynthetic capacity, non-structural carbohydrate (NSC) accumulation, and remobilisation. Four soybean cultivars were cultivated in open-top chambers at two CO2 levels. Photosynthesis rates were determined from R2 to R6. Plants were sampled at R5 and R8 to determine carbohydrate concentrations. There were significant variations in yield responses among the soybean cultivars under e[CO2], from no change in DS1 to a 22% increase in SN14. DS1 and SN14 had the smallest and largest increase, respectively, in daily carbon assimilation capacity. Under e[CO2], DS1, MF5, and XHJ had an increase in Ci, at which point the transition from Rubisco-limited to ribulose-1,5-bisphosphate regeneration-limited photosynthesis occurred, in contrast with SN14. Thus, the cultivars might have distinct mechanisms that enhance photosynthesis under e[CO2] conditions. A positive correlation was between daily carbon assimilation response to e[CO2] and soybean yield, emphasising the importance of enhanced photosynthate accumulation before the R5 stage in determining yield response to e[CO2]. E[CO2] significantly influenced NSC accumulation in vegetative organs at R5, with variation among cultivars. There was enhanced NSC remobilisation during seed filling, indicating cultivar-specific responses to the remobilisation of sucrose and soluble sugars, excluding sucrose and starch. A positive correlation was between leaf and stem NSC remobilisation and yield response to e[CO2], emphasising the role of genetic differences in carbohydrate remobilisation mechanisms in determining soybean yield variation under elevated CO2 levels.

SETD7 Promotes Cell Proliferation and Migration via Methylation-mediated TAF7 in Clear Cell Renal Cell Carcinoma.

SET domain containing 7(SETD7), a member of histone methyltransferases, is abnormally expressed in multiple tumor types. However, the biological function and underlying molecular mechanism of SETD7 in clear cell renal cell carcinoma (ccRCC) remain unclear. Here, we explored the biological effects of SETD7-TAF7-CCNA2 axis on proliferation and metastasis in ccRCC. We identified both SETD7 and TAF7 were up-regulated and significantly promoted the proliferation and migration of ccRCC cells. Concurrently, there was a significant positive correlation between the expression of SETD7 and TAF7, and the two were colocalized in the nucleus. Mechanistically, SETD7 methylates TAF7 at K5 and K300 sites, resulting in the deubiquitination and stabilization of TAF7. Furthermore, re-expression of TAF7 could partially restore SETD7 knockdown inhibited ccRCC cells proliferation and migration. In addition, TAF7 transcriptionally activated to drive the expression of cyclin A2 (CCNA2). And more importantly, the methylation of TAF7 at K5 and K300 sites exhibited higher transcriptional activity of CCNA2, which promotes formation and progression of ccRCC. Our findings reveal a unique mechanism that SETD7 mediated TAF7 methylation in regulating transcriptional activation of CCNA2 in ccRCC progression and provide a basis for developing effective therapeutic strategies by targeting members of SETD7-TAF7-CCNA2 axis.

Transition of intracranial aneurysmal wall enhancement from high to low wall shear stress mediation with size increase: A hemodynamic study based on 7T magnetic resonance imaging.

Background: Wall shear stress (WSS) has been proved to be related to the formation, development and rupture of intracranial aneurysms. Aneurysm wall enhancement (AWE) on magnetic resonance imaging (MRI) can be caused by inflammation and have confirmed its relationship with low WSS. High WSS can also result in inflammation but the research of its correlation with AWE is lack because of the focus on large aneurysms limited by 3T MRI in most previous studies.This study aimed to assess the potential association between high or low WSS and AWE in different aneuryms. Especially the relationship between high WSS and AWE in small aneurysm. Methods: Forty-three unruptured intracranial aneurysms in 42 patients were prospectively included for analysis. 7.0 T MRI was used for imaging. Aneurysm size was measured on three-dimensional time-of-flight (TOF) images. Aneurysm-to-pituitary stalk contrast ratio (CRstalk) was calculated on post-contrast black-blood T1-weighted fast spin echo sequence images. Hemodynamics were assessed by four-dimensional flow MRI. Results: The small aneurysms group had more positive WSS-CRstalk correlation coefficient distribution (dome: 78.6 %, p = 0.009; body: 50.0 %, p = 0.025), and large group had more negative coefficient distribution (dome: 44.8 %, p = 0.001; body: 69.0 %, p = 0.002). Aneurysm size was positively correlated with the significant OSI-CRstalk correlation coefficient at the dome (p = 0.012) and body (p = 0.010) but negatively correlated with the significant WSS-CRstalk correlation coefficient at the dome (p < 0.001) and body (p = 0.017). Conclusion: AWE can be mediated by both high and low WSS, and translate from high WSS- to low WSS-mediated pathways as size increase. Additionally, AWE may serve as an indicator of the stage of aneurysm development via different correlations with hemodynamic factors.

Personalized venlafaxine dose prediction using artificial intelligence technology: a retrospective analysis based on real-world data.

BACKGROUND: Venlafaxine dose regimens vary considerably between individuals, requiring personalized dosing. AIM: This study aimed to identify dose-related influencing factors of venlafaxine through real-world data analysis and to construct a personalized dose model using advanced artificial intelligence techniques. METHOD: We conducted a retrospective study on patients with depression treated with venlafaxine. Significant variables were selected through a univariate analysis. Subsequently, the predictive performance of seven models (XGBoost, LightGBM, CatBoost, GBDT, ANN, TabNet, and DT) was compared. The algorithm that demonstrated optimal performance was chosen to establish the dose prediction model. Model validation used confusion matrices and ROC analysis. Additionally, a dose subgroup analysis was conducted. RESULTS: A total of 298 patients were included. TabNet was selected to establish the venlafaxine dose prediction model, which exhibited the highest performance with an accuracy of 0.80. The analysis identified seven crucial variables correlated with venlafaxine daily dose, including blood venlafaxine concentration, total protein, lymphocytes, age, globulin, cholinesterase, and blood platelet count. The area under the curve (AUC) for predicting venlafaxine doses of 75 mg, 150 mg, and 225 mg were 0.90, 0.85, and 0.90, respectively. CONCLUSION: We successfully developed a TabNet model to predict venlafaxine doses using real-world data. This model demonstrated substantial predictive accuracy, offering a personalized dosing regimen for venlafaxine. These findings provide valuable guidance for the clinical use of the drug.

Trefoil factor 3 can stimulate Th17 cell response in the development of type 2 diabetes mellitus.

This study aims to evaluate the role of trefoil factor 3 (TFF3) peptides in type 2 diabetes mellitus (T2DM) from an inflammatory perspective. The focus was on exploring how TFF3 affects the function of T cells. TFF3 overexpression model was constructed using lentivirus in Jurkat cell lines. We evaluated the impact of TFF3 on the proliferation, apoptosis, and IL-17A levels of Jurkat cells cultured in high glucose. The T2DM model was induced in TFF3 knockout (KO) mice through streptozotocin combined with high-fat diet. The measurements included glucose tolerance, insulin tolerance, inflammation markers, Th17 cell proportion, and pancreatic pathological changes. The T2DM modeling led to splenomegaly in mice, and increased expression of TFF3 in their spleens. Overexpression of TFF3 increased the proportion of IL-17+ T cells and the levels of Th17-related cytokines in Jurkat cells. There was no difference in body weight and blood glucose levels between wild-type and TFF3 KO mice. However, T2DM mice lacking the TFF3 gene showed improved glucose utilization, ameliorated pancreatic pathology, decreased inflammation levels, and reduced Th17 cell ratio. TFF3 may be involved in the chronic inflammatory immune response in T2DM. Its mechanism may be related to the regulation of the RORγt/IL-17 signaling pathway and its impact on T cell proliferation and apoptosis.

Parallel event-triggered dynamic output feedback control for nonlinear networked systems with randomly occurring multiple communication delays.

This paper investigates the issue of parallel event-triggered (PET) dynamic output feedback control for networked control systems (NCSs) built by the discrete-time T-S fuzzy model. Initially, a novel PET dynamic output feedback controller is designed. Based on saving network resources and enhancing transmission efficiency, the PET strategy makes full use of relative and absolute triggering condition information. And the dynamic output feedback control can not only address unmeasurable states but also provide a better response to the internal information of the system. The random multiple communication delays and the ℓth-order Rice fading model with different channel coefficients, meanwhile, are both applied in the system. It is closer to the actual situation. Subsequently, new sufficient conditions of membership function dependence are proposed via the staircase function approximation method combined with Lyapunov stability. It guarantees that the system is exponentially mean square stable (EMSS) with H∞ performance. Ultimately, the presented results are validated using two examples. In the future, we will explore the correlative research of T-S fuzzy Markov jump NCSs.

Developing a machine learning model for predicting venlafaxine active moiety concentration: a retrospective study using real-world evidence.

BACKGROUND: Venlafaxine is frequently prescribed for patients with depression. To control the concentration of venlafaxine within the therapeutic window for the best treatment effect, a model to predict venlafaxine concentration is necessary. AIM: Our objective was to develop a prediction model for venlafaxine concentration using real-world evidence based on machine learning and deep learning techniques. METHOD: Patients who underwent venlafaxine treatment between November 2019 and August 2022 were included in the study. Important variables affecting venlafaxine concentration were identified using a combination of univariate analysis, sequential forward selection, and machine learning techniques. Predictive performance of nine machine learning and deep learning algorithms were assessed, and the one with the optimal performance was selected for modeling. The final model was interpreted using SHapley Additive exPlanations. RESULTS: A total of 330 eligible patients were included. Five influential variables that affect venlafaxine concentration were venlafaxine daily dose, sex, age, hyperlipidemia, and adenosine deaminase. The venlafaxine concentration prediction model was developed using the eXtreme Gradient Boosting algorithm (R2 = 0.65, mean absolute error = 77.92, root mean square error = 93.58). In the testing cohort, the accuracy of the predicted concentration within ± 30% of the actual concentration was 73.49%. In the subgroup analysis, the prediction accuracy was 69.39% within the recommended therapeutic range of venlafaxine concentration within ± 30% of the actual value. CONCLUSION: The XGBoost model for predicting blood concentration of venlafaxine using real-world evidence was developed, guiding the adjustment of regimen in clinical practice.

MyoD1 promotes the transcription of BIK and plays an apoptosis-promoting role in the development of gastric cancer.

Myogenic differentiation (MyoD) 1, which is known as a pivotal transcription factor during myogenesis, has been proven dysregulated in several cancers. However, litter is known about the precise role and downstream genes of MyoD1 in gastric cancer (GC) cells. Here, we report that MyoD1 is lowly expressed in primary GC tissues and cells. In our experiments, overexpression of MyoD1 inhibited cell proliferation. Downstream genes of MyoD1 regulation were investigated using RNA-Seq. As a result, 138 up-regulated genes and 20 down-regulated genes and 27 up-regulated lncRNAs and 20 down-regulated lncRNAs were identified in MyoD1 overexpressed MKN-45 cells, which participated in epithelial cell signaling in Helicobacter pylori infection, glycosaminoglycan biosynthesis (keratan sulfate), notch signaling pathway, and others. Among these genes, BIK was directly regulated by MyoD1 in GC cells and inhibited cancer cell proliferation. The BIK knockdown rescued the effects of MyoD1 overexpression on GC cells. In conclusion, MyoD1 inhibited cell proliferation via 158 genes and 47 lncRNAs downstream directly or indirectly that participated in multiple signaling pathways in GC, and among these, MyoD1 promotes BIK transcription by binding to its promoter, then promotes BIK-Bcl2-caspase 3 axis and regulates GC cell apoptosis.

Fecal Microbiota Transplantation Improves Clinical Symptoms of Fibromyalgia: An Open-Label, Randomized, Nonplacebo-Controlled Study.

Fibromyalgia (FM) is a complex and poorly understood disorder characterized by chronic and widespread musculoskeletal pain, of which the etiology remains unknown. Now, the disorder of the gut microbiome is considered as one of the main causes of FM. This study aimed to investigate the potential benefits of fecal microbiota transplantation (FMT) in patients with FM. A total of 45 patients completed this open-label, randomized, nonplacebo-controlled clinical study. The numerical rating scale scores in the FMT group were slightly lower than the control group at 1 month (P > .05), and they decreased significantly at 2, 3, 6, and 12 months after treatment (P < .001). Besides, compared with the control group, the Widespread Pain Index, Symptom Severity, Hospital Anxiety and Depression Scale, and Pittsburgh Sleep Quality Index scores were significantly lower in the FMT group at different time points (P < .001). After 6 months of treatment, there was a significant increase in serotonin (5-hydroxytryptamine) and gamma-aminobutyric acid levels (P < .001), while glutamate levels significantly decreased in the FMT group (P < .001). The total effective rate was higher in the FMT group (90.9%) compared to the control group (56.5%) after 6 months of treatment (P < .05). FMT can effectively improve the clinical symptoms of FM. With the close relations between the changes in neurotransmitters and FM, certain neurotransmitters may serve as a diagnostic marker or potential target for FM patients. PERSPECTIVE: FMT is a novel therapy that aims to restore the gut microbial balance and modulate the gut-brain axis. It is valuable to further explore the therapeutic effect of FMT on FM. Furthermore, certain neurotransmitters may become a diagnostic marker or a new therapeutic target for FM patients.

Intravenous immunoglobulin alleviates Japanese encephalitis virus-induced peripheral neuropathy by inhibiting the ASM/ceramide pathway.

Japanese encephalitis virus (JEV) infection is considered a global public health emergency. Severe peripheral neuropathy caused by JEV infection has increased disability and mortality rates in recent years. Because there are very few therapeutic options for JEV infection, prompt investigations of the ability of clinically safe, efficacious and globally available drugs to inhibit JEV infection and ameliorate peripheral neuropathy are urgently needed. In this study, we found that high doses of intravenous immunoglobulin, a function inhibitor of acid sphingomyelinase (FIASMA), inhibited acid sphingomyelinase (ASM) and ceramide activity in the serum and sciatic nerve of JEV-infected rats, reduced disease severity, reversed electrophysiological and histological abnormalities, significantly reduced circulating proinflammatory cytokine levels, inhibited Th1 and Th17 cell proliferation, and suppressed the infiltration of inflammatory CD4 + cells into the sciatic nerve. It also maintained the peripheral nerve-blood barrier without causing severe clinical side effects. In terms of the potential mechanisms, ASM was found to participate in immune cell differentiation and to activate immune cells, thereby exerting proinflammatory effects. Therefore, immunoglobulin is a FIASMA that reduces abnormal immune responses and thus targets the ASM/ceramide system to treat peripheral neuropathy caused by JEV infection.

Type I/II Immune Balance Contributes to the Protective Effect of AIF-1 on Hepatic Immunopathology Induced by Schistosoma japonicum in a Transgenic Mouse Model.

Schistosomiasis is the second most debilitating neglected tropical disease in the world. Liver egg granuloma and fibrosis are the main damage of schistosomiasis. In this study, the role of allograft inflammatory factor-1 (AIF-1) in liver pathology and its regulation in immune responses were investigated in a transgenic mouse infected with Schistosoma japonicum. We found that AIF-1 overexpression reduced worm burden and decreased egg granuloma sizes and serum alanine aminotransferase levels, along with inhibited hepatic collagen deposition and serum hydroxyproline levels during S. japonicum infection. Moreover, AIF-1 overexpression resulted in an increased ratio of Th1/Th2, increased levels of IFN-γ and T-bet, and lower levels of GATA-3 in the spleen, accompanied by increased M1 percentages, decreased M2 percentages, and thus a higher ratio of M1/M2 in the peritoneal cavity and liver. AIF-1 induced CD68 and iNOS mRNA expression and protein levels of cytoplasmic p-P38 and nuclear NF-κB, along with enhanced levels of TNF-α and TGF-ß in macrophages in vitro. Moreover, the hepatic pathology had a negative correlation with Th1/Th2 and M1/M2 ratios in the infected mice. The findings reveal that the beneficial role of AIF-1 in alleviating hepatic damage is related to restoring type I/II immune balance in S. japonicum infection.

Machine learning-based prediction of sertraline concentration in patients with depression through therapeutic drug monitoring.

Background: Sertraline is a commonly employed antidepressant in clinical practice. In order to control the plasma concentration of sertraline within the therapeutic window to achieve the best effect and avoid adverse reactions, a personalized model to predict sertraline concentration is necessary. Aims: This study aimed to establish a personalized medication model for patients with depression receiving sertraline based on machine learning to provide a reference for clinicians to formulate drug regimens. Methods: A total of 415 patients with 496 samples of sertraline concentration from December 2019 to July 2022 at the First Hospital of Hebei Medical University were collected as the dataset. Nine different algorithms, namely, XGBoost, LightGBM, CatBoost, random forest, GBDT, SVM, lasso regression, ANN, and TabNet, were used for modeling to compare the model abilities to predict sertraline concentration. Results: XGBoost was chosen to establish the personalized medication model with the best performance (R 2 = 0.63). Five important variables, namely, sertraline dose, alanine transaminase, aspartate transaminase, uric acid, and sex, were shown to be correlated with sertraline concentration. The model prediction accuracy of sertraline concentration in the therapeutic window was 62.5%. Conclusion: In conclusion, the personalized medication model of sertraline for patients with depression based on XGBoost had good predictive ability, which provides guidance for clinicians in proposing an optimal medication regimen.

The mechanism of anthracene degradation by tryptophan -2,3-dioxygenase (T23D) in Comamonas testosteroni.

It is well known that anthracene is a persistent organic pollutant. Among the four natural polycyclic aromatic hydrocarbons (PAHs) degrading strains, Comamonas testosterone (CT1) was selected as the strain with the highest degradation efficiency. In the present study, prokaryotic transcriptome analysis of CT1 revealed an increase in a gene that encodes tryptophane-2,3-dioxygenase (T23D) in the anthracene and erythromycin groups compared to CK. Compared to the wild-type CT1 strain, anthracene degradation by the CtT23D knockout mutant (CT-M1) was significantly reduced. Compared to Escherichia coli (DH5α), CtT23D transformed DH5α (EC-M1) had a higher degradation efficiency for anthracene. The recombinant protein rT23D oxidized tryptophan at pH 7.0 and 37 °C with an enzyme activity of 2.42 ± 0.06 µmol min-1·mg-1 protein. In addition, gas chromatography-mass (GC-MS) analysis of anthracene degradation by EC-M1 and the purified rT23D revealed that 2-methyl-1-benzofuran-3-carbaldehyde is an anthracene metabolite, suggesting that it is a new pathway.

A sharp and selective fluorescence paper-based sensor based on inner filter effect for ratiometric detection of four Sudan dyes in food matrix.

The addition of Sudan dyes with carcinogenic effects to food threatens human health. Herein, a ratiometric fluorescence strip consisting of core-shell upconversion particles (NaYF4:Yb,Tm@NaYF4:Yb,Er), metal-organic frameworks and dual-template molecularly imprinted polymers was developed to selectively and sensitively detect four Sudan dyes based on inner filter effect (detection time only takes 8 min). The high adsorption capacity of metal-organic frameworks and the greater overlap between the emission of NaYF4:Yb,Tm@NaYF4:Yb,Er and the absorbance of four Sudan dyes enable the signal responses to be more sensitive. The limits of detection in chilli powder samples are as low as 29.87 ng/g, 37.55 ng/g, 47.89 ng/g and 51.02 ng/g, with satisfactory recovery (93.32-103.4%) and minor relative standard deviations (≤4.3%). This method broadens the idea for low-cost and portable detection of multiple illegal additives in complex substrates with high selectivity and sensitivity based on one kind of fluorescent strip.

IL-8 from CD248-expressing cancer-associated fibroblasts generates cisplatin resistance in non-small cell lung cancer.

Chemotherapy-resistant non-small cell lung cancer (NSCLC) presents a substantial barrier to effective care. It is still unclear how cancer-associated fibroblasts (CAFs) contribute to NSCLC resistance to chemotherapy. Here, we found that CD248+ CAFs released IL-8 in NSCLC, which, in turn, enhanced the cisplatin (CDDP) IC50 in A549 and NCI-H460 while decreasing the apoptotic percentage of A549 and NCI-H460 in vitro. The CD248+ CAFs-based IL-8 secretion induced NSCLC chemoresistance by stimulating nuclear factor kappa B (NF-κB) and elevating ATP-binding cassette transporter B1 (ABCB1). We also revealed that the CD248+ CAFs-based IL-8 release enhanced cisplatin chemoresistance in NSCLC mouse models in vivo. Relative to wild-type control mice, the CD248 conditional knockout mice exhibited significant reduction of IL-8 secretion, which, in turn, enhanced the therapeutic efficacy of cisplatin in vivo. In summary, our study identified CD248 activates the NF-κB axis, which, consecutively induces the CAFs-based secretion of IL-8, which promotes NSCLC chemoresistance. This report highlights a potential new approach to enhancing the chemotherapeutic potential of NSCLC-treating cisplatin.

Tailoring the Position of Ester Group on N-Alkyl Chains of Benzotriazole-based Small Molecule Acceptors for High-Performance Organic Solar Cells.

Side chain engineering plays a vital role in exploring high-performance small molecule acceptors (SMAs) for organic solar cells (OSCs). In this work, we designed and synthesized a series of A-DA'D-A type SMAs by introducing different N-substituted alkyl and ester alkyl side chains on benzotriazole (BZ) central unit and aimed to investigate the effect of different ester substitution positions on photovoltaic performances. All the new SMAs with ester groups exhibit lower the lowest unoccupied molecular orbital (LUMO) energy levels and more blue-shifted absorption, but relatively higher absorption coefficients than alkyl chain counterpart. After blending with the donor PM6, the ester side chain-based devices demonstrate enhanced charge mobility, reduced amorphous intermixing domain size and long-lived charge transfer state compared to the alkyl chain counterpart, which are beneficial to achieve higher short-circuit current density (Jsc ) and fill factor (FF), simultaneously. Thereinto, the PM6 : BZ-E31 based device achieves a higher power conversion efficiency (PCE) of 18.33 %, which is the highest PCE among the OSCs based on the SMAs with BZ-core. Our work demonstrated the strategy of ester substituted side chain is a feasible and effective approach to develop more efficient SMAs for OSCs.