International Journal of Biological Sciences最新文献

The Role of Thrombospondins in Osteoarthritis: from Molecular Mechanisms to Therapeutic Potential.

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-03-03 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.103343

Yirixiati Aihaiti, Hui Yu, Peng Xu

{"title":"The Role of Thrombospondins in Osteoarthritis: from Molecular Mechanisms to Therapeutic Potential.","authors":"Yirixiati Aihaiti, Hui Yu, Peng Xu","doi":"10.7150/ijbs.103343","DOIUrl":"10.7150/ijbs.103343","url":null,"abstract":"Osteoarthritis (OA) is a prevalent chronic degenerative joint disorder characterized by cartilage degeneration, joint inflammation, and pain. The pathogenesis of OA still remains unclear. Among the various factors contributing to OA, the role of extracellular matrix (ECM) proteins, particularly thrombospondins (TSPs), has garnered significant attention. TSPs, a family of multifunctional extracellular matrix glycoproteins, are known to participate in numerous physiological and pathological processes, including cell adhesion, migration, differentiation, angiogenesis, and synaptogenesis through cell-cell and cell-matrix interactions. In this review, we provide a summary of the current understanding of TSP proteins in the pathogenesis of OA, including their effects on cartilage homeostasis, synovial inflammation, and subchondral bone remodeling and arthritic pain. We also review the evidence supporting the potential of TSP proteins as diagnostic biomarkers and therapeutic targets, with a focus on recent advances in cartilage regeneration, gene delivery therapy and pain management. Considering the multifaceted roles of TSP proteins in maintaining articular homeostasis, TSP proteins emerge as promising therapeutic targets for OA.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 5","pages":"2346-2359"},"PeriodicalIF":8.2,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dysregulation of N-glycosylation by Rpn1 knockout in spermatocytes induces male infertility via endoplasmic reticulum stress in mice.

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-03-03 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.106468

Mingyu Zhang, Mengjing Li, Hanzhen Li, Yanling Wan, Shuang Yang, Shuhui Ji, Haobo Zhang, Chao Liu, Gang Lu, Xiaohua Jiang, Hongbin Liu

{"title":"Dysregulation of N-glycosylation by Rpn1 knockout in spermatocytes induces male infertility via endoplasmic reticulum stress in mice.","authors":"Mingyu Zhang, Mengjing Li, Hanzhen Li, Yanling Wan, Shuang Yang, Shuhui Ji, Haobo Zhang, Chao Liu, Gang Lu, Xiaohua Jiang, Hongbin Liu","doi":"10.7150/ijbs.106468","DOIUrl":"10.7150/ijbs.106468","url":null,"abstract":"N-glycosylation protein modification plays a crucial regulatory role in numerous biological processes, although their contribution to male reproduction in mammals remains largely undefined. Here, we found that Ribophorin I (RPN1), a subunit of oligosaccharyltransferase complex, is indispensable for spermatogenesis in male germ cells. Germ cell-specific Rpn1 knockout results in significant inhibition of the progression of meiosis, consequently disrupting homologous chromosome pairing, meiotic recombination, and DNA double strand breaks repair during meiosis. N-glycoproteomic profiling revealed that glycosylation levels are reduced in endoplasmic reticulum-associated proteins, while functional analyses showed that Rpn1 deficiency could inhibit endoplasmic reticulum function and trigger endoplasmic reticulum stress during meiosis and increasing apoptosis levels in mice. These findings highlight the essential physiological functions of N-glycosylation modification in male spermatogenesis and expand our understanding of its role in male fertility.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 5","pages":"2360-2379"},"PeriodicalIF":8.2,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Functions and Clinical Applications of Exosomes in Gastric Cancer.

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-02-28 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.98087

Zhi Zheng, Yuhao Zhai, Xiaosheng Yan, Zimeng Wang, Haiqiao Zhang, Rui Xu, Xiaoye Liu, Jun Cai, Zhongtao Zhang, Yuxi Shang, Jun Zhang, Jie Yin

{"title":"Functions and Clinical Applications of Exosomes in Gastric Cancer.","authors":"Zhi Zheng, Yuhao Zhai, Xiaosheng Yan, Zimeng Wang, Haiqiao Zhang, Rui Xu, Xiaoye Liu, Jun Cai, Zhongtao Zhang, Yuxi Shang, Jun Zhang, Jie Yin","doi":"10.7150/ijbs.98087","DOIUrl":"10.7150/ijbs.98087","url":null,"abstract":"Gastric cancer is a common and highly invasive type of malignant tumor, the pathogenesis of which remains unclarified. However, exosomes are now known to play important roles in gastric cancer development and treatment. Cells use exosomes for the packaging and transportation of a variety of bioactive molecules, such as proteins, double-stranded DNA, and micro-ribonucleic acids, to other sites. Exosome-specific membrane structures and exosomal contents are widely involved in processes that facilitate material exchange and intercellular communication between gastric cancer cells. They help in forming a pre-metastatic microenvironment, promoting the proliferation and apoptosis of gastric cancer cells, and driving invasion, metastasis, and resistance to anti-tumor drugs. In this review, we aimed to summarize the findings of research articles indexed in the PubMed, Web of Science, and Embase databases and published up to May 31, 2024, on the role of exosomes in the pathogenesis of gastric cancer and their potential clinical applications in its treatment. Thus, research on exosomes may lead to breakthroughs in the early diagnosis of gastric cancer and identification of novel treatments.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 5","pages":"2330-2345"},"PeriodicalIF":8.2,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neutrophils in tumor- and inflammation-induced lymphangiogenesis.

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-02-26 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.103458

Xinyu Li, Xiaoxin Liu, Haotian Wei, Yanyan Liu, Gang Xu

引用次数: 0

OLFML3 Promotes IRG1 Mitochondrial Localization and Modulates Mitochondrial Function in Macrophages.

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-02-26 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.103859

Qijun Yu, Hong Mei, Qian Gu, Ran Zeng, Yanan Li, Junjie Zhang, Chenxu Gao, Hai Fang, Jieming Qu, Jia Liu

{"title":"OLFML3 Promotes IRG1 Mitochondrial Localization and Modulates Mitochondrial Function in Macrophages.","authors":"Qijun Yu, Hong Mei, Qian Gu, Ran Zeng, Yanan Li, Junjie Zhang, Chenxu Gao, Hai Fang, Jieming Qu, Jia Liu","doi":"10.7150/ijbs.103859","DOIUrl":"10.7150/ijbs.103859","url":null,"abstract":"Olfactomedin-like protein 3 (OLFML3), belonging to olfactomedin (OLF) protein family, has poorly defined functions. Recent studies have reported the functions of OLFML3 in anti-viral immunity and tumorigenesis. In this study, we investigated the roles of OLFML3 in macrophages. In LPS- or Pseudomonas aeruginosa-induced acute lung injury (ALI) mouse model, OLFML3 depletion exacerbated inflammatory response, leading to reduced survival. OLFML3 achieved the in vivo activity by regulating macrophage phagocytosis and migration. Mass spectrometry analysis revealed immunoresponsive gene 1 (IRG1) as an OLFML3-interacting protein. IRG1 is a mitochondrial decarboxylase that catalyzes the conversion of cis-aconitate to itaconate, a myeloid-borne mitochondrial metabolite with immunomodulatory activities. Further investigation showed that OLFML3 could prevent LPS-induced mitochondrial dysfunction in macrophages by maintaining the homeostasis of mitochondrial membrane potential (MMP), mitochondrial reactive oxygen species (mtROS) and itaconate-related metabolites. In-depth protein-protein interaction studies showed that OLFML3 could promote IRG1 mitochondrial localization via a mitochondrial transport protein, apoptosis inducing factor mitochondria associated 1 (AIFM1). In summary, our study showed that OLFML3 could facilitate IRG1 mitochondrial localization and prevent LPS-induced mitochondrial dysfunction in macrophages.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 5","pages":"2275-2295"},"PeriodicalIF":8.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of the LCOR-PLCL1 pathway that restrains lipid accumulation and tumor progression in clear cell renal cell carcinoma.

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-02-26 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.107981

Wen Li, Jian Shi, Qingyang Lv, Daojia Miao, Diaoyi Tan, Xiaojun Lu, Hairong Xiong, Qianqian Luo, Yaru Xia, Yuqi Han, Xuejiao Dong, Guixiao Huang, Xiaoping Zhang, Hongmei Yang

{"title":"Identification of the LCOR-PLCL1 pathway that restrains lipid accumulation and tumor progression in clear cell renal cell carcinoma.","authors":"Wen Li, Jian Shi, Qingyang Lv, Daojia Miao, Diaoyi Tan, Xiaojun Lu, Hairong Xiong, Qianqian Luo, Yaru Xia, Yuqi Han, Xuejiao Dong, Guixiao Huang, Xiaoping Zhang, Hongmei Yang","doi":"10.7150/ijbs.107981","DOIUrl":"10.7150/ijbs.107981","url":null,"abstract":"Clear cell renal cell carcinoma (ccRCC) is the typical pathological subtype of renal cell carcinoma (RCC), representing about 80% of RCC. Reprogramming of lipid metabolism is one of the nonnegligible pathogeneses in ccRCC. Currently, the underlying regulatory mechanisms of lipid metabolism in ccRCC remain inadequately understood. In this study, we performed bioinformatics analyses and experiments both in vivo and in vitro to explore the biological functions and specific mechanisms of the ligand dependent nuclear receptor corepressor LCOR in ccRCC. Mechanistically, RUNX1 was a transcriptional suppressor of PLCL1, LCOR could interact with RUNX1 to relieve RUNX1-mediated repression of PLCL1, leading to increased PLCL1 expression, which, in turn, inhibited the tumor progression and lipid accumulation in ccRCC. Furthermore, PLCL1 decreased lipid accumulation through UCP1-mediated lipid browning and facilitated tumor apoptosis by activating p38 phosphorylation. In conclusion, the LCOR-RUNX1-PLCL1 axis provides a novel molecular mechanism underlying the progression and lipid storage of ccRCC. LCOR modulation represents a potential therapeutic strategy for the treatment in ccRCC.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 5","pages":"2296-2312"},"PeriodicalIF":8.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Remote Ischemic Preconditioning Attenuates Mitochondrial Dysfunction and Ferroptosis of Tubular Epithelial Cells by Inhibiting NOX4-ROS Signaling in Acute Kidney Injury.

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-02-26 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.105667

Wei Wei, Letian Yang, Bo Wang, Lei Tang, Jian Li, Caihong Liu, Yongxiu Huang, Zhuyun Zhang, Dingkun Zhang, Ling Zhang, Liang Ma, Ping Fu, Yuliang Zhao

{"title":"Remote Ischemic Preconditioning Attenuates Mitochondrial Dysfunction and Ferroptosis of Tubular Epithelial Cells by Inhibiting NOX4-ROS Signaling in Acute Kidney Injury.","authors":"Wei Wei, Letian Yang, Bo Wang, Lei Tang, Jian Li, Caihong Liu, Yongxiu Huang, Zhuyun Zhang, Dingkun Zhang, Ling Zhang, Liang Ma, Ping Fu, Yuliang Zhao","doi":"10.7150/ijbs.105667","DOIUrl":"10.7150/ijbs.105667","url":null,"abstract":"Acute kidney injury (AKI) is a worldwide clinical burden associated with high morbidity and mortality. Remote ischemic preconditioning (rIPC), a brief nonlethal ischemia and reperfusion (IR) in remote tissues or limbs, has been used in an attempt to protect against AKI, but its underlying signaling pathways has not been elucidated. In the present study, rIPC protected kidney function and pathological injury and mitigated NADPH oxidase 4 (NOX4) upregulation in different AKI models (cisplatin, LPS and IRI). Furthermore, rIPC significantly attenuated mitochondrial dysfunction and ameliorated tubular epithelial ferroptosis during AKI. Mechanistically, in wild-type AKI mice and TCMK-1 cells, rIPC effectively decreased kidney ROS production, preserved mitochondrial dynamics and mitophagy, and ameliorated tubular epithelial ferroptosis. Notably, these protective effects of rIPC were further enhanced by NOX4 knockout or silencing and mitigated by NOX4 overexpression. Our study showed that rIPC may attenuate mitochondrial dysfunction and ferroptosis in tubular epithelial cells in AKI by inhibiting NOX4-ROS signaling. NOX4 might be used as a biomarker for monitoring the biological effects of rIPC to optimize the rIPC protocol and facilitate future translational studies.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 5","pages":"2313-2329"},"PeriodicalIF":8.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PSMC6 regulation of ovarian cancer cisplatin resistance unravels a new mode for proteasome targeting.

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-02-26 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.104612

Matteo Costantino, Luca Mirra, Padraig D'arcy, Cristina Corno, Nives Carenini, Elisabetta Corna, Johannes Gubat, Chiara M Ciniselli, Pietro Pratesi, Paolo Verderio, Stig Linder, Giovanni L Beretta, Paola Perego

{"title":"PSMC6 regulation of ovarian cancer cisplatin resistance unravels a new mode for proteasome targeting.","authors":"Matteo Costantino, Luca Mirra, Padraig D'arcy, Cristina Corno, Nives Carenini, Elisabetta Corna, Johannes Gubat, Chiara M Ciniselli, Pietro Pratesi, Paolo Verderio, Stig Linder, Giovanni L Beretta, Paola Perego","doi":"10.7150/ijbs.104612","DOIUrl":"10.7150/ijbs.104612","url":null,"abstract":"Ovarian carcinoma has still a poor prognosis. CRISPR/Cas9 loss-of-function screen revealed a relationship between the PSMC6 proteasome subunit expression and survival of cisplatin-sensitive and -resistant ovarian carcinoma cells. Increased levels of PSMC6 were evidenced in multiple ovarian carcinoma cell lines versus normal cells. An association between PSMC6 levels and tumour stages as well as with a reduced progression-free survival was found. Since a PSMC6 interactome analysis evidenced limited knowledge on PSMC6 biology, mechanistic studies were carried out. PSMC6 knockdown indicated reduced cell growth and clonogenicity in cisplatin-sensitive IGROV-1 and -resistant IGROV-1/Pt1 cells, with a higher impact in resistant cells. This behaviour was accompanied by the accumulation of ubiquitinated proteins and down-regulation of ERK1/2 phosphorylation mediated by increased DUSP6. PSMC6 silencing increased sensitivity to cisplatin in IGROV-1/Pt1 cells as shown by clonogenic assay and 3D spheroids. Since PSMC6 knockdown did not change sensitivity to 20S and 19S proteasome inhibitors, we suggest a new mode of proteasome targeting by interference with a proteasome ATPase. Overall, a link between PSMC6 and ovarian carcinoma aggressiveness is envisioned, highlighting PSMC6 as a potential diagnostic and therapeutic target.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 5","pages":"2258-2274"},"PeriodicalIF":8.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Harnessing Macrophages in Cancer Therapy: from Immune Modulators to Therapeutic Targets.

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-02-26 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.106275

Huabing Tan, Meihe Cai, Jincheng Wang, Tao Yu, Houjun Xia, Huanbin Zhao, Xiaoyu Zhang

{"title":"Harnessing Macrophages in Cancer Therapy: from Immune Modulators to Therapeutic Targets.","authors":"Huabing Tan, Meihe Cai, Jincheng Wang, Tao Yu, Houjun Xia, Huanbin Zhao, Xiaoyu Zhang","doi":"10.7150/ijbs.106275","DOIUrl":"10.7150/ijbs.106275","url":null,"abstract":"Macrophages, as the predominant phagocytes, play an essential role in pathogens defense and tissue homeostasis maintenance. In the context of cancer, tumor-associated macrophages (TAMs) have evolved into cunning actors involved in angiogenesis, cancer cell proliferation and metastasis, as well as the construction of immunosuppressive microenvironment. Once properly activated, macrophages can kill tumor cells directly through phagocytosis or attack tumor cells indirectly by stimulating innate and adaptive immunity. Thus, the prospect of targeting TAMs has sparked significant interest and emerged as a promising strategy in immunotherapy. In this review, we summarize the diverse roles and underlying mechanisms of TAMs in cancer development and immunity and highlight the TAM-based therapeutic strategies such as inhibiting macrophage recruitment, inhibiting the differentiation reprogramming of TAMs, blocking phagocytotic checkpoints, inducing trained macrophages, as well as the potential of engineered CAR-armed macrophages in cancer therapy.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 5","pages":"2235-2257"},"PeriodicalIF":8.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular Mechanisms of Ischemia/Reperfusion Injury and Graft Dysfunction in Liver Transplantation: Insights from Multi-Omics Studies in Rodent Animal Models.

IF 8.2 2区生物学

International Journal of Biological Sciences Pub Date : 2025-02-24 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.109449

Zhengtao Liu, Jun Xu, Ting Que, Shuping Que, Luca Valenti, Shusen Zheng

{"title":"Molecular Mechanisms of Ischemia/Reperfusion Injury and Graft Dysfunction in Liver Transplantation: Insights from Multi-Omics Studies in Rodent Animal Models.","authors":"Zhengtao Liu, Jun Xu, Ting Que, Shuping Que, Luca Valenti, Shusen Zheng","doi":"10.7150/ijbs.109449","DOIUrl":"10.7150/ijbs.109449","url":null,"abstract":"Rodent ischemia-reperfusion injury (IRI) and liver transplantation (LT) models play crucial roles in mimicking graft injury and immune rejection, developing therapeutic approaches, and evaluating the efficacy of treatments. The application of integrated multi-omics data and advanced omics techniques like single-cell RNA sequencing in rodent models has expanded researchers' perspectives on pathophysiological processes in LT settings. This review summarizes key molecules and pathways associated with reperfusion injury and prognosis in LT models, highlighting the potential of omics data in understanding and improving transplant outcomes. In addition, we highlight the current challenges and future approaches for the application of omics data in rodent LT models. Cross-species validation with human data will improve therapeutic potential. Finally, further applications combining advanced single-cell, spatial omics technologies and machine learning algorithms will help to identify the key regulatory networks in specific cell populations underlying poor outcomes after LT.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 5","pages":"2135-2154"},"PeriodicalIF":8.2,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0