Applied Biochemistry and Biotechnology最新文献

{"title":"Upregulated PCSK9 Level Contributes to Human Pulmonary Microvascular Endothelial Cell Apoptosis in Cigarette Smoke Extract-Induced COPD Models Through TLR4/NF-kappaB Pathway Activation.","authors":"Yunxia Li, Fengzhen He, Shasha Zhao, Chunli Zhang, Xueyang Chen, Xiang Luo","doi":"10.1007/s12010-025-05328-8","DOIUrl":"https://doi.org/10.1007/s12010-025-05328-8","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) is persistent and can result in irreversible alveolar collapse and increase the risk of cardiovascular disease. PCSK9 belongs to the pro-protein convertase family and is capable of modulating cholesterol metabolism and low-density lipoprotein (LDL). PCSK9 is associated with endothelial dysfunction and its suppression is conducive to vascular function. The aim of this study was to explore PCSK9 expression in the lung tissues of patients with COPD and investigate the regulation of PCSK9 in cigarette smoke extract (CSE)-exposed human pulmonary microvascular endothelial cells (HPMECs) and an in vivo cigarette smoke (CS)-exposed mouse model. PCSK9 is drastically upregulated in the lung tissues of patients with COPD relative to those of individuals who have never smoked. PCSK9 expression in HPMECs and the CS-exposed mouse model was found to increase. Functional assays demonstrated that PCSK9 silencing decreased CS-induced lung injury and neutrophil and macrophage infiltration. PCSK9 silencing also abolished CSE-induced apoptosis by upregulating Bcl-2 and downregulating Bax expression in COPD mice and cell models. PCSK9 silencing alleviated the inflammatory response in the BALF of CS-exposed mice and CSE-treated HPMECs. The protein expression of P65, NLRP3, ASC, TLR4, p-P65, MyD88, and caspase-1 in mouse BALF and HPMECs was inhibited after PCSK9 knockdown. Collectively, these observations indicate the important role of PCSK9 in COPD progression and present promising treatment targets for COPD.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astragalus Polysaccharides Alleviate Sepsis by Boosting Adrenal Hormone Synthesis and Repairing Microvascular Damage.","authors":"Yihui Chai, Yunzhi Chen, Zhaoxia Huang, Xiaoqing Liu, Jun Li","doi":"10.1007/s12010-025-05332-y","DOIUrl":"https://doi.org/10.1007/s12010-025-05332-y","url":null,"abstract":"<p><p>Sepsis is a severe infection-related condition commonly seen in clinical practice, characterized by systemic inflammation and multi-organ dysfunction. Astragalus polysaccharides (APS), the primary bioactive compound from the traditional Chinese herb Astragalus, has shown significant anti-inflammatory, immunomodulatory, and antioxidant effects. This study aimed to explore APS's potential in alleviating sepsis by enhancing adrenal cortical hormone production and repairing adrenal microvascular damage, while uncovering the underlying molecular mechanisms. Using an SD rat model, sepsis was induced via cecal ligation and puncture (CLP) surgery. Rats were treated with APS at doses of 400, 600, or 800 mg/kg/day for 7 days. Survival rates, inflammatory cytokine levels, adrenal function, and molecular pathways were evaluated using techniques such as ELISA, HE staining, TUNEL assay, metabolomics, transcriptome sequencing, and validation. Results showed that APS significantly reduced sepsis-induced mortality, elevated serum cortisol levels, and lowered inflammatory cytokines IL-6 and TNF-α. Histological analysis revealed that APS protected the adrenal cortex from apoptosis and inflammatory infiltration. Metabolomic analysis identified 154 differentially regulated metabolites, including significant changes in steroid hormones. Transcriptomic sequencing indicated changes in gene expression, suggesting that APS may inhibit NF-κB activity and promote nitric oxide (NO) production, thus protecting endothelial cells. These findings suggest that APS improves adrenal function and mitigates sepsis-related damage, offering promising therapeutic avenues for sepsis treatment.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liposomal Delivery of Allolobophora caliginosa Coelomic Fluid Attenuates Myocardial Infarction by Suppressing Oxidative Damage, Inflammation, and Apoptosis.","authors":"Asmaa E Farouk, Sohair R Fahmy, Amel M Soliman, Sherif Abdelaziz Ibrahim, Shimaa A Sadek","doi":"10.1007/s12010-025-05340-y","DOIUrl":"https://doi.org/10.1007/s12010-025-05340-y","url":null,"abstract":"<p><p>Myocardial infarction (MI) is a concerning coronary heart disease with increasing rates of death and morbidity worldwide. One potential approach to prevent MI involves exploring invertebrate supplements within the nanoliposome formulation to improve targeted delivery, thereby mitigating MI-induced heart damage. Therefore, the study aimed to evaluate the cardioprotective efficacy of liposomal delivery of Allolobophora caliginosa coelomic fluid (ACCF-liposomes) on adrenaline-induced MI in rats. Thirty male albino rats were allocated into five groups: Control, Untreated MI, MI-treated ACCF, MI-treated free liposomes, and MI-treated ACCF-liposomes. The treatment regimen spanned 21 days. Electrocardiography (ECG), biochemical, oxidative stress, inflammatory mediators, electrolyte balance, histopathological and immunohistochemical analyses, and DNA fragmentation were evaluated. Liposomal delivery of ACCF has shown promise in regulating ECG criteria and reducing myocardial markers, particularly AST, LDH, MMP-2, creatine kinase, and troponin-I. It also improves lipid metabolism and inhibits myocardial oxidative stress. Additionally, ACCF and ACCF-liposomes treatment improves cardiomyocyte architecture and reduces DNA fragmentation in myocardial infarcted rats. Furthermore, encapsulating ACCF within liposomes statistically reduced the expression of iNOS and Beclin-1 in cardiac tissue. This suggests that liposomal delivery of ACCF enhances its effectiveness in treating myocardial infarction, potentially via its antioxidant, anti-inflammatory, and anti-apoptotic attributes.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hexanoic Acid Production from Chinese Cabbage Waste Driven by In Situ Lactic Acid Pre-Fermentation: Effect of pH.","authors":"Zhengang Chen, Liu Huang, Xiaofeng Ji, Ranran Chen, Jiying Zhu","doi":"10.1007/s12010-025-05334-w","DOIUrl":"https://doi.org/10.1007/s12010-025-05334-w","url":null,"abstract":"<p><p>Chain elongation (CE) with lactic acid as electron donor is an important way for the biosynthesis of hexanoic acid, and pH is crucial for the carbon flow direction in the CE process. In this study, a high concentration of lactic acid was achieved through the pre-fermentation of Chinese cabbage wastes (CCW), and the effects of pH on the metabolic flow of lactic acid and hexanoic acid yield during CE reaction were investigated. The coexistence of Lactobacillus, Caproiciproducens, and Acinetobacter at pH 5.5 facilitated the CE process driven by lactic acid, obtaining the highest hexanoic acid yield of 5.01 ± 0.01 g COD/L. At pH 6.0, the high abundance of propionic acid-producing bacteria, such as Blautia and Succiniclasticum, converted lactic acid to propionic acid via the acrylate pathway, resulting in low selectivity of hexanoic acid. Without pH control, acetic acid was the main product due to the low pH at the initial stage of fermentation.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improving the Accumulation and Solubility of Human Interferon-γ (hIFN-γ) in Escherichia coli: A Fusion Protein-Based Method and Network Pharmacology Analysis.","authors":"Narjes Akbari, Raheem Haddad, Reza Heidari-Japelaghi, Nematollah Gheibi","doi":"10.1007/s12010-025-05331-z","DOIUrl":"https://doi.org/10.1007/s12010-025-05331-z","url":null,"abstract":"<p><p>Using a network pharmacology-based method, some differentially expressed genes (DEGs) were detected in the colon cancer cell line (HCT116) after treatment with the human interferon-γ (hIFN-γ). Moreover, several pathways including cell cycle, NOD-like receptor signaling pathway, and P53 signaling pathway were identified, indicating the inhibitory effect of IFN-γ on the growth and proliferation of HCT116 cells. To validate in silico results, the hIFN-γ was first produced in Escherichia coli strain Rosetta and its bioactivity was then analyzed by anticancer assay. The production of hIFN-γ was performed via the optimization of several effective factors and the fusion of hIFN-γ to elastin like-polypeptide (ELP) tag. The highest amount of hIFN-γ (3.87 ± 0.37% of total soluble protein) was obtained at 22 °C with OD₆₀₀ = 0.6 and IPTG = 0.25 after 3-h inoculation. Whereas, the highest level of the hIFN-γ-ELP, about 4.58 ± 0.14% of TSP, was observed after 6-h inoculation. Compared to the hIFN-γ, the amount of hIFN-γ-ELP accumulation in the form of soluble increased significantly by more than 18%, proposing the desirable effect of ELP on the accumulation and solubility of hIFN-γ. Furthermore, the hIFN-γ prohibited the growth and proliferation of the HCT116 cells and the highest level of inhibition of cell proliferation was found at a concentration of 32.00 pg/mL hIFN-γ after 72-h incubation. Anticancer activity of hIFN-γ was also confirmed through the expression analysis of Bax, p53, and Bcl-2, suggesting the cytotoxic role of hIFN-γ toward HCT116 cells via inducing apoptosis process and arresting cell cycle.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TCF4 Promotes Neuroblastoma Proliferation and Inhibits Ferroptosis by Transactivating GPX4 Expression.","authors":"Yingming Wang, Qiang Gao, Xin Chen, Qian Dong, Ruihong Luan, Fujiang Li, Hongting Lu, Xianjun Zhou","doi":"10.1007/s12010-025-05329-7","DOIUrl":"https://doi.org/10.1007/s12010-025-05329-7","url":null,"abstract":"<p><p>Neuroblastoma, an aggressive pediatric malignancy, exhibits aberrant expression of transcription factors implicated in tumor progression. Here, we investigated the functional role of transcription factor 4 (TCF4) in neuroblastoma, focusing on its impact on cellular proliferation and ferroptosis-a regulated form of iron-dependent cell death, and elucidated the underlying molecular mechanism. Firstly, the expressions of TCF4 in neuroblastoma tissues and cell lines were analyzed, and the expressions of TCF4 mRNA and protein were significantly up-regulated. Functional analysis demonstrated that sh-TCF4 could significantly proliferate neuroblastoma cells, which was measured by CCK-8 kit, EdU staining, and clone formation experiments. Concurrently, TCF4 knockdown significantly elevated ROS accumulation and lipid peroxidation levels. Besides, sh-TCF4 decreased the levels of FTH1 and increased the TFR1 expression. Mechanistically, bioinformatic analysis using the JASPAR database predicted TCF4 binding sites within GPX4 promoter, a key ferroptosis regulator. ChIP and dual-luciferase reporter assays confirmed direct TCF4 occupancy and transcriptional activation of GPX4. Rescue experiments further validated the axis, as GPX4 overexpression abrogated the anti-proliferative and pro-ferroptotic effects induced by sh-TCF4. Collectively, the findings revealed TCF4 as a critical promoter of neuroblastoma growth and ferroptosis resistance, acting through direct up-regulation of GPX4. Targeting the TCF4-GPX4 axis may offer a novel therapeutic strategy to enhance ferroptosis sensitivity in neuroblastoma, warranting further preclinical exploration.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asiaticoside Mitigates Chronic Obstructive Pulmonary Disease by Modulating TRIM27 Stability and Activating PGC-1α/Nrf2 Signaling.","authors":"Feng Zhu, Yuxian Ji, Qian You, Qigang Dong, Yao Tang, Yu Zhang","doi":"10.1007/s12010-025-05288-z","DOIUrl":"https://doi.org/10.1007/s12010-025-05288-z","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease and is pathologically associated with epithelial-mesenchymal transition (EMT) and mitochondrial dysfunction. Asiaticoside (AS) has shown significant anti-inflammatory effects in a variety of diseases. Herein, the pharmacological influences of AS in COPD were probed. COPD mice were exposed to cigarette smoke (CS), and BEAS-2B cells were treated with cigarette smoke extract (CSE) for in vitro studies. HE staining was performed to assess lung pathological alters. The role of AS on inflammation, apoptosis, EMT, and mitochondrial dysfunction was analyzed by ELISA assay, western blot, Flow cytometry, DCFH-DA staining, and JC-1 staining. TRIM27 m6A expression was measured by MeRIP assay. The relationship between YTHDF1, TRIM27, and PGC-1α was determined by Co-IP or RIP assays. AS treatment relieved CSE-triggered inflammation, apoptosis, EMT, and mitochondrial dysfunction in a dose-dependent manner. Mechanically, AS suppressed PGC-1α ubiquitination degradation by reducing TRIM27 level in an m6A-YTHDF1-dependent manner. As expected, the mitigatory effect of AS on CSE-triggered BEAS-2B cell damage was abrogated by TRIM27 addition. Further, TRIM27 addition abrogated the restoring effect of AS on CS-caused pulmonary pathological damage in COPD mice. AS alleviated COPD by activating PGC-1α/Nrf2 signaling through weakening TRIM27 stability in an m6A-YTHDF1-dependent manner.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficient Detection of N-sialoglycans in N-glycomics Using Mass Spectrometry by nMatch.","authors":"Shanshan Zhao, Shouwen Du, Yudong Guan, Hartmut Schlüter","doi":"10.1007/s12010-025-05337-7","DOIUrl":"https://doi.org/10.1007/s12010-025-05337-7","url":null,"abstract":"<p><p>The structural instability and electronegativity of sialic acids make N-sialoglycan profiling challenging. We compared commonly used preparation strategies, including native, acetohydrazide-based derivatization, and permethylation, in N-glycomics with nMatch, an R-based bioinformatics tool that ensures full coverage of the detected N-glycans using mass spectrometry. We demonstrated that permethylation leads to efficient detection of not only N-sialoglycans but also other N-glycans and, therefore, provides a valuable reference for the selection of the appropriate N-glycan preparation strategy in future studies.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144635873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Peptide Derived from Casein Hydrolysates as a Growth Factor for Lactobacillus delbrueckii subsp. bulgaricus sp1.1.","authors":"Xinyue Hao, Xiaoning Song, Jing Ren, Olayemi Eyituoyo Dudu, Jingya Jiang, Jianhua Zeng, Song Wang, Huaxi Yi, Lanwei Zhang, Pimin Gong","doi":"10.1007/s12010-025-05339-5","DOIUrl":"https://doi.org/10.1007/s12010-025-05339-5","url":null,"abstract":"<p><p>Milk proteins are traditionally recognized as nitrogen sources that support lactic acid bacteria (LAB) proliferation. Notably, oligopeptides may serve as the primary nitrogen source, and have the potential of enhancing the resistance of microbial strains to acidic environments. In this study, the impact of various casein hydrolysates on the proliferation of L. delbrueckii subsp. bulgaricus sp1.1 and the composition of peptides was studied. This study unveiled a novel peptide, KEGIHAQ, with a significant capacity to enhance both acid tolerance and proliferation of LAB. Inclusion of 0.1% (w/v) KEGIHAQ increased the number of viable bacteria by 1.68 times compared with the control and attained 1.34 × 10⁹ CFU/mL, and under acid stress, the number of viable bacteria was 1.41 times that of the control. Transcriptomic analysis revealed that KEGIHAQ was not directly assimilated by L. delbrueckii subsp. bulgaricus sp1.1; instead, it acted as an effector, which upregulated the dipeptide transporter protein DppA and amino acid metabolism genes. This facilitated dipeptide uptake, amino acid synthesis, energy generation, and various bacterial physiological activities, while enhancing bacterial acid resistance mechanisms. These results provided valuable insights in identifying target peptides for nitrogen sources in future LAB high-density cultures, whether through biosynthesis or chemical synthesis.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144615701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"hsa_circ_0004771-Targeted Adsorption of miR-429 Mediates ATP2A2 Expression to Attenuate Endoplasmic Reticulum Stress and Mitochondrial Dysfunction During Myocardial Infarction.","authors":"Ying Deng, Ya Wu, SongChun Liu, YiJun Hou","doi":"10.1007/s12010-025-05310-4","DOIUrl":"https://doi.org/10.1007/s12010-025-05310-4","url":null,"abstract":"<p><p>Circular RNAs (circRNAs) have emerged as key regulators of cardiovascular pathophysiology. This study intended to mechanistically dissect the role of hsa_circ_0004771 in MI pathogenesis. An in vivo MI mouse model was established, and mouse cardiomyocytes (HL-1 cells) were cultured under hypoxic conditions to construct an in vitro cardiomyocyte injury model. Cardiac function in mice was assessed; serum markers of myocardial injury were quantified. Pathological alterations and levels of apoptosis in myocardial tissues were examined. Key oxidative stress indicators and pro-inflammatory cytokines were detected. Cell viability, cytotoxicity, and apoptosis were evaluated. Endoplasmic reticulum stress (ERS)-related proteins and mitochondrial function were analyzed. Serum samples from acute myocardial infarction (AMI) patients were collected for the detection of hsa_circ_0004771, miR-429, and ATPase sarcoplasmic/endoplasmic reticulum Ca²⁺ transporting 2(ATP2A2) mRNA expression levels. Furthermore, dual-luciferase reporter assays and RNA pull-down assays were utilized to validate the interactions between miR-429 and circ_0004771 or ATP2A2. Circ_0004771 expression was significantly downregulated in AMI patients and experimental models. Overexpression of circ_0004771 improved cardiac function, ameliorated myocardial injury, decreased infarct size, suppressed oxidative stress markers, and attenuated inflammatory cytokine levels in MI mice. In vitro studies demonstrated that circ_0004771 overexpression alleviated hypoxia-induced injury in HL-1 cardiomyocytes, concurrently mitigating ERS, mitochondrial dysfunction, and calcium overload. Mechanistically, circ_0004771 acted as a sponge of miR-429, thereby upregulating ATP2A2 expression. Inhibition of miR-429 attenuated hypoxia-induced cardiomyocyte damage, while miR-429 overexpression reversed the protective effects of circ_0004771. Silencing of ATP2A2 abrogated the therapeutic benefits of miR-429 inhibition. Circ_0004771 mitigates hypoxia-induced ERS, mitochondrial dysfunction, and calcium overload via the miR-429/ATP2A2 axis in MI.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}