Cell Biology International最新文献

Macrophage Protein Disulfide Isomerase Increases Infection by Leishmania amazonensis.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-04-03 DOI: 10.1002/cbin.70020

Guilherme M P Carrara, Guilherme A Souza-Silva, Tania C B D Reis, Bruna C D Alencar, Silvia B Boscardin, Peter E Kima, Beatriz S Stolf

{"title":"Macrophage Protein Disulfide Isomerase Increases Infection by Leishmania amazonensis.","authors":"Guilherme M P Carrara, Guilherme A Souza-Silva, Tania C B D Reis, Bruna C D Alencar, Silvia B Boscardin, Peter E Kima, Beatriz S Stolf","doi":"10.1002/cbin.70020","DOIUrl":"https://doi.org/10.1002/cbin.70020","url":null,"abstract":"Leishmania spp. are protozoans with a digenetic life cycle responsible for causing tegumentary and visceral leishmaniasis. Leishmania (L.) amazonensis is the second most prevalent dermotropic species in Brazil. Infection in humans and other mammals takes place when phagocytes, mainly macrophages, uptake the parasite. Many proteins on the phagocytic cell surface participate in Leishmania phagocytosis. In this study, we evaluated the role of surface protein disulfide isomerase (PDI) in phagocytosis and infection of macrophages by L. amazonensis. PDI is the second most abundant chaperone in the endoplasmic reticulum. A unique study in the literature associated the presence of PDI on the macrophage surface with increased phagocytosis by Leishmania (L.) infantum (syn L. chagasi), the species most frequently associated with visceral leishmaniasis in the Americas. In the present work we evaluated L. amazonensis infections in transgenic FVB/NJ mice overexpressing PDI (TgPDIA1). We validated the presence of PDI on their macrophages surface by flow cytometry. We demonstrated that infection of macrophages pretreated with anti-PDI antibodies was lower compared to control cells. Accordingly, we showed that the overexpression of PDI increased the adhesion of parasites and infection of macrophages. We also demonstrated that macrophages overexpressing PDI internalize more zymosan particles. In vivo imaging of infections with luciferase-expressing parasites in wild-type and TgPDIA1 mice indicated that the overexpression of PDI was not associated with significant differences in footpad lesions and parasite burden, probably due to the ubiquitous overexpression of PDI and the roles of this molecule in other immune system functions.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Induction of Ferroptosis by Shikonin in Gastric Cancer via the DLEU1/mTOR/GPX4 Axis.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-03-24 DOI: 10.1002/cbin.70018

Yiying Wang, Midie Xu, Cheng Liu, Xin Wang, Xiaoyan Zhang, Weiqi Sheng, Xiaoyu Wang

{"title":"Induction of Ferroptosis by Shikonin in Gastric Cancer via the DLEU1/mTOR/GPX4 Axis.","authors":"Yiying Wang, Midie Xu, Cheng Liu, Xin Wang, Xiaoyan Zhang, Weiqi Sheng, Xiaoyu Wang","doi":"10.1002/cbin.70018","DOIUrl":"https://doi.org/10.1002/cbin.70018","url":null,"abstract":"Gastric cancer (GC) is the most prevalent cancer in Asia. Shikonin, one of the ingredients extracted from the roots of Lithospermum erythrorhizon, has been proven to be a necrosis inducer and has an antitumour effect on many cancers. We explored the mechanism of the antitumour effect of shikonin in GC. CCK8 and clonogenic assays were used to determine the effect of shikonin on the proliferation of GC cell lines. Shikonin could induce reactive oxygen species (ROS), lipid ROS, intracellular ferrous iron (Fe2+), and malondialdehyde (MDA) in GC. We also found that shikonin decreased the expression of GPX4 by suppressing GPX4 synthesis and decreasing ferritin. Furthermore, long noncoding RNA deleted in lymphocytic leukaemia 1 (DLEU1) is an oncogene in GC, and shikonin decreased DLEU1 expression in GC cells. Overexpression of DLEU1 eliminated the anticancer effect of shikonin. Mechanistically, shikonin might decrease GPX4 levels by inhibiting the DLEU1/mTOR pathway. DLEU1 was sponged with miR-9-3p, which also regulated mTOR and GPX4. A xenograft tumour model of GC was established, and shikonin treatment inhibited cell proliferation and induced ferroptosis. In conclusion, shikonin exerts its antitumour effects on GC by triggering ferroptosis, and the DLEU1/mTOR/GPX4 axis may play an essential role in shikonin-induced ferroptosis. Therefore, our findings provide a potential lead compound for treating GC.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of Potential Targets Associated With Programmed Cell Death for Acute Kidney Injury Based on WGCNA.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-03-21 DOI: 10.1002/cbin.70019

Yu Wang, Bo Deng, Yu Pan, Feng Ding

{"title":"Identification of Potential Targets Associated With Programmed Cell Death for Acute Kidney Injury Based on WGCNA.","authors":"Yu Wang, Bo Deng, Yu Pan, Feng Ding","doi":"10.1002/cbin.70019","DOIUrl":"https://doi.org/10.1002/cbin.70019","url":null,"abstract":"Programmed cell death (PCD) pathways play a crucial role in maintaining normal cell turnover and tissue homeostasis, encompassing apoptosis and regulated necrosis. However, the involvement of PCD in the pathogenesis of acute kidney disease remains unexplored. In this study, we utilized gene expression profiling datasets (GSE139061) obtained from the Gene Expression Omnibus (GEO) database. Through differential gene expression analysis and weighted gene co-expression network analysis (WGCNA), we identified five key genes associated with PCD, namely DPP4, ATF3, KIT, MSX1, and SNAI2 in acute kidney injury (AKI). Subsequently, single sample gene set enrichment analysis (ssGSEA) was employed to demonstrate the correlation between these five hub genes and immune cell infiltration as well as activation of immune pathways. Furthermore, we validated our findings by analyzing gene expression patterns using a mouse model of ischemia-reperfusion injury. In conclusion, our study is the first to propose the concept of PCD in the pathogenesis of AKI. This finding has significant implications for future investigations into pro-inflammatory immune mechanisms mediated by damage-associated molecular patterns (DAMPs) during the stages of AKI. Our findings underscore the necessity for further investigation into these molecules, which may offer new avenues for therapeutic intervention in AKI. These identified genes may serve as promising targets for intervention in cases of acute kidney diseases.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exposure of Bisphenols (BPA, BPB and BPC) in HepG2 Cells Results in Lysosomal Dysfunction and Lipid Accumulation. 双酚（BPA、BPB 和 BPC）暴露于 HepG2 细胞会导致溶酶体功能紊乱和脂质积累。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-03-18 DOI: 10.1002/cbin.70017

Kiran Gill, Eshika Bindal, Parul Garg, Deepak Kumar, Rajasri Bhattacharyya, Dibyajyoti Banerjee

引用次数: 0

Piwei Peiyuan Prescription Attenuates the Progression of Chronic Atrophic Gastritis by Eliciting MAPK10-Mediated Mitochondrial Autophagy.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-03-18 DOI: 10.1002/cbin.70016

Yi Zhang, Ying Wu, Bei Pei, Qin Sun, Cheng Zhang, Qi Yang, Yueping Jin, Jing Wu, Xuejun Li

{"title":"Piwei Peiyuan Prescription Attenuates the Progression of Chronic Atrophic Gastritis by Eliciting MAPK10-Mediated Mitochondrial Autophagy.","authors":"Yi Zhang, Ying Wu, Bei Pei, Qin Sun, Cheng Zhang, Qi Yang, Yueping Jin, Jing Wu, Xuejun Li","doi":"10.1002/cbin.70016","DOIUrl":"https://doi.org/10.1002/cbin.70016","url":null,"abstract":"Piwei Peiyuan (PWPY) prescription is a traditional Chinese medicine prescription and has been efficiently used in the clinics to treat chronic atrophic gastritis (CAG) for many years. However, the mechanism of action underlying PWPY for treating CAG remains elusive. A CAG rat animal and cell model was constructed in this study to explore the action mechanism of PWPY prescription in treating CAG. Here we show that PWPY attenuates the progression of CAG by eliciting MAPK10-mediated mitochondrial autophagy. Experimental model of CAG was introduced using N-methyl-n'-nitro-n-nitroguanidine (MNNG). Our histological analyses reveal that MNNG-induced CAG in rat undergoes classical morphological alterations judged by immunohistochemistry and serum level of PGⅠ, PGⅡ, and G17. Importantly, PWPY treatment prevents the progression of MNNG-induced CAG judged by serum level of PGⅠ, PGⅡ, and G17. Interestingly, PWPY treatment inhibits MAPK10 activity judged by biochemical assays and promotes mitochondrial autophagy judged by electron microscopic analyses. Thus, we conclude that PWPY attenuates the progression of MNNG-induced CAG and prevents precancerous lesions by harnessing MAPK10-elicited mitochondrial autophagy. The MNNG-induced experimental CAG model provides a robust platform for further delineating therapeutic targets underlying PWPY regimen.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cellular and Molecular Mechanisms of Phytochemicals Against Inflammation-Associated Diseases and Viral Infection.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-03-16 DOI: 10.1002/cbin.70011

Zhaodi Zheng, Junying Gao, Yubing Ma, Xitan Hou

{"title":"Cellular and Molecular Mechanisms of Phytochemicals Against Inflammation-Associated Diseases and Viral Infection.","authors":"Zhaodi Zheng, Junying Gao, Yubing Ma, Xitan Hou","doi":"10.1002/cbin.70011","DOIUrl":"https://doi.org/10.1002/cbin.70011","url":null,"abstract":"Inflammation-associated diseases have become widespread and pose a significant threat to human health, and the therapeutic methods for diverse diseases are inadequate due to the undesirable effects of synthetic ingredients. Recently, more and more evidence indicated that phytochemicals, plant secondary metabolites, have numerous therapeutic functions against human diseases via affecting a variety of mechanisms with their distinct advantages of high efficiency and low toxicity. Here, we highlight the mechanisms of phytochemicals to hinder inflammation-associated diseases (including Inflammatory diseases, cardiovascular diseases, metabolic syndrome, neurological disorders, skin diseases, respiratory diseases, kidney diseases, gastrointestinal diseases, retinal diseases, viral infections) by regulating the crosstalk among various signal cascades (including MicroRNAs, SIRT1, DNMTs, NF-κB, NLRP3, TGF-β, the Gasdermin-mediated pyroptosis pathway), which can be considered as a novel and potential therapeutic strategy. Furthermore, phytochemicals could prevent virus infection by disturbing different targets in the virus replication cycle. However, natural plants have shown limited bioavailability due to their low water solubility, the use of adjuvants such as liposomal phytochemicals, phytochemical nanoparticles and phytochemicals-phospholipid complex promote their bioavailability to exhibit beneficial effects against various diseases. The purpose of this review is to explore the molecular mechanisms and promising applications of phytochemicals in the fields of inflammation-associated diseases and virus infection to provide some direction.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

FLOT1 Is a Novel Serum Biomarker of Ovarian Cancer Targeted by N6-methyladenosine Modification Inhibition.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-03-11 DOI: 10.1002/cbin.70015

Bin Guan, Qi Lu, Junyu Chen, Jingyi Fang, Zhenyu Liu, Wei Li, Lingyun Zhang, Guoxiong Xu

{"title":"FLOT1 Is a Novel Serum Biomarker of Ovarian Cancer Targeted by N6-methyladenosine Modification Inhibition.","authors":"Bin Guan, Qi Lu, Junyu Chen, Jingyi Fang, Zhenyu Liu, Wei Li, Lingyun Zhang, Guoxiong Xu","doi":"10.1002/cbin.70015","DOIUrl":"https://doi.org/10.1002/cbin.70015","url":null,"abstract":"Ovarian cancer (OC) is a deadly disease and lacks a precise marker for diagnosis worldwide. Our previous work has shown the overexpression of flotillin-1 (FLOT1) in OC tissue. To improve diagnostic sensitivity and accuracy, we evaluated the serum level of FLOT1 in OC patients and found that the serum concentration of FLOT1 as well as CA125 was significantly increased in patients with OC compared with healthy control (p < 0.01) and those with benign tumors (p < 0.05). The detection rate (above the upper limit of a cut-off value) of FLOT1 and CA125 was 77.78% and 72.22%, respectively, in patients with OC, which was increased to 88.89% in combination. The elevation of FLOT1 was confirmed in the serum of nude mice after the implantation of human OC cells. A high level of FLOT1 protein in the serum was positively correlated with the overexpression of FLOT1 protein in OC tissues. Furthermore, the level of m6A modification of FLOT1 mRNA was significantly high in OC cells compared with normal ovarian epithelial cells, leading to an increase in FLOT1 mRNA expression. Application of a methylation inhibitor, 3-deazaadenosine, decreased FLOT1 mRNA expression in OC cells and suppressed tumor formation in a xenograft mouse model. In conclusion, the current study demonstrated that FLOT1 is a novel serum biomarker of OC and can be targeted by m6A modification inhibition. These data highlight the potential application of FLOT1 as a diagnostic marker and a therapeutic target for patients with OC.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PRKCQ Is Dispensable for Spermatogenesis in Mice.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-03-07 DOI: 10.1002/cbin.70014

Yu Chen, Hong Chen, Zhongyan Han, Yiqiang Cui, Chenghao Situ, Yaling Qi, Qing Cheng, Yan Li

{"title":"PRKCQ Is Dispensable for Spermatogenesis in Mice.","authors":"Yu Chen, Hong Chen, Zhongyan Han, Yiqiang Cui, Chenghao Situ, Yaling Qi, Qing Cheng, Yan Li","doi":"10.1002/cbin.70014","DOIUrl":"https://doi.org/10.1002/cbin.70014","url":null,"abstract":"Protein kinase C (PKC) family is evolutionally conserved and involved in various signaling cascades in all cells. Of the family, PRKCQ is dominatingly expressed in testis, however, its molecular functionality in spermatogenesis and male fertility remains unclear. To evaluate the role of PRKCQ in spermatogenesis, Prkcq knockout mice were generated using CRISPR/Cas9 system. Histological and immunofluorescence assays by different markers were employed to assess the testicular cells variation. Sperm parameters were analyzed by computer-assisted sperm analyzer. qPCR assay was used to examine the expression levels of other PKC family genes. We found that PRKCQ was conserved throughout evolution and highly expressed in testis. Prkcq-/- mice were successfully generated and developed viably. Normal fertility was observed in Prkcq-/- males. Prkcq-/- mice exhibited no defects in spermatogenic cells and mature sperm were full in epididymis. Furthermore, there were no differences in sperm motility and progressive motility between Prkcq-/- males and controls. Our findings report a detailed phenotypic analysis of Prkcq-/- males and indicate that PRKCQ is not required for spermatogenesis in male mice, which can provide basic information for other researchers.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Proteomics Profiling Reveals the Neuroprotective Effects of Melatonin on Exogenous β-amyloid-42 Induced Mitochondrial Impairment, Intracellular β-amyloid Accumulation and Tau Hyperphosphorylation in Human SH-SY5Y Cells.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-03-06 DOI: 10.1002/cbin.70013

Jiraporn Panmanee, Matthew Phanchana, Phorutai Pearngam, Nopphon Petchyam, Kornkanok Promthep, Ponlawit Wisomka, Suchanoot Kutpruek, Supitcha Pannengpetch, Tanya Prasertporn, Sujira Mukda, Piyarat Govitrapong, Chutikorn Nopparat

{"title":"A Proteomics Profiling Reveals the Neuroprotective Effects of Melatonin on Exogenous β-amyloid-42 Induced Mitochondrial Impairment, Intracellular β-amyloid Accumulation and Tau Hyperphosphorylation in Human SH-SY5Y Cells.","authors":"Jiraporn Panmanee, Matthew Phanchana, Phorutai Pearngam, Nopphon Petchyam, Kornkanok Promthep, Ponlawit Wisomka, Suchanoot Kutpruek, Supitcha Pannengpetch, Tanya Prasertporn, Sujira Mukda, Piyarat Govitrapong, Chutikorn Nopparat","doi":"10.1002/cbin.70013","DOIUrl":"https://doi.org/10.1002/cbin.70013","url":null,"abstract":"Alzheimer's disease (AD) is prevalent in the elderly population and characterized by the intracellular accumulation of neurofibrillary tangles (NFTs), composed of tau proteins, and extracellular deposition of beta-amyloid protein (Aβ). The present study aimed to investigate the neuroprotective effects of melatonin on Aβ42-induced AD-like pathology in SH-SY5Y cell lines. To assess the effects of melatonin on Aβ42-exposed cells, we performed a proteomics analysis of altered protein expression in Aβ42-treated cells, with or without melatonin Pretreatment, using label-free nano-LC-MS/MS. Experimental validations of pathways related to the neuroprotective effects of melatonin were carried out using Milliplex amyloid beta and tau magnetic bead assays, Western blot analysis, and measurements of mitochondrial membrane potential and ROS levels. Our results show that Aβ42 exposure led to an increase in an accumulation of intracellular Aβ42/40 and phosphorylated tau (Thr181)/Tau ratios. Pretreatment with melatonin effectively reduced the levels of these pathogenic proteins. Proteomics analysis has revealed protein markers associated with the Alzheimer's disease pathway, neuronal synapses, cellular apoptosis, and mitochondrial functions. Changes in proteins regulating the mitochondrial permeability transition pore, the electron transport chain, and mitochondrial oxidative stress were observed in Aβ42-treated cells. Pretreatment with melatonin protected the cells against Aβ42-induced cellular damages by regulating the expression of several proteins underpinning these biological processes, including the suppression of mitochondrial ROS generation and mitigation of mitochondrial membrane depolarization.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dysregulation of Calcium Homeostasis: An Important Factor Leading to Ferroptosis in Cardiovascular Diseases.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-03-05 DOI: 10.1002/cbin.70012

Yifan Zhang, Leiyin Zheng, Tongtong Che, Ning Meng

{"title":"Dysregulation of Calcium Homeostasis: An Important Factor Leading to Ferroptosis in Cardiovascular Diseases.","authors":"Yifan Zhang, Leiyin Zheng, Tongtong Che, Ning Meng","doi":"10.1002/cbin.70012","DOIUrl":"https://doi.org/10.1002/cbin.70012","url":null,"abstract":"Cardiovascular disease is a circulatory system disease involving the heart and blood vessels, which is one of the main causes of human health loss and even life-threatening. Ca2+ is an important signal molecule. Free calcium ions in the cytoplasm are involved in various physiological and biochemical reactions of cells. Ferroptosis is a programmed cell death driven by lipid peroxidation dependent on free ferrous ions. The essence of ferroptosis is the accumulation of lipid peroxide caused by the increase of intracellular ferrous ion content, which leads to the damage of the phospholipid membrane and eventually cell death. Studies have shown that calcium homeostasis and ferroptosis are involved in the occurrence and development of cardiovascular diseases, but the relationship between them remains to be clarified. This article reviews the various pathways regulating calcium homeostasis in cells and the occurrence and development mechanism of ferroptosis, and discusses the relationship between the two in cardiovascular diseases, which is expected to provide novel and important strategies for alleviating and treating cardiovascular diseases.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0