Antioxidants最新文献

{"title":"Environmental Toxins and Oxidative Stress: The Link to Cardiovascular Diseases.","authors":"Rasheed O Sule, Gabriela Del Toro Rivera, Tanishq Vaidya, Emily Gartrell, Aldrin V Gomes","doi":"10.3390/antiox14050604","DOIUrl":"10.3390/antiox14050604","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) remain a leading global health concern, responsible for substantial morbidity and mortality. In recent years, as our understanding of the multifaceted nature of CVDs has increased, it has become increasingly evident that traditional risk factors alone do not account for the entirety of cardiovascular morbidity and mortality. Environmental toxins, a heterogeneous group of substances ubiquitous in our surroundings, have now entered the spotlight as offenders in the development and progression of CVDs. Environmental toxins include heavy metals, air pollutants, pesticides, and endocrine-disrupting chemicals, among others. Upon exposure, they can elicit oxidative stress, a condition characterized by an imbalance between the production of reactive oxygen species (ROS) and the body's ability to detoxify and repair the resulting damage. Oxidative stress triggers a cascade of events, including inflammation, endothelial dysfunction, lipid peroxidation, and vascular remodeling, which can contribute to the development of atherosclerosis, hypertension, and other cardiovascular pathologies. This article delves into the molecular mechanisms underpinning oxidative stress-mediated cardiovascular damage induced by environmental toxins, emphasizing the role of specific toxins in this process. Further research is necessary to understand how individual susceptibility and genotype influence the impact of environmental toxins on oxidative stress and the risk of CVD.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New Perspectives on Postmenopausal Osteoporosis: Mechanisms and Potential Therapeutic Strategies of Sirtuins and Oxidative Stress.","authors":"Huiying Zhao, Fan Yu, Wei Wu","doi":"10.3390/antiox14050605","DOIUrl":"10.3390/antiox14050605","url":null,"abstract":"<p><p>Estrogen levels are the core factor influencing postmenopausal osteoporosis (PMOP). Estrogen can affect the progression of PMOP by regulating bone metabolism, influencing major signaling pathways related to bone metabolism, and modulating immune responses. When estrogen levels decline, the activity of Sirtuins (SIRTs) is reduced. SIRTs are enzymes that function as NAD+-dependent deacetylases. SIRTs can modulate osteocyte function, sustain mitochondrial homeostasis, and modulate relevant signaling pathways, thereby improving bone metabolic imbalances, reducing bone resorption, and promoting bone formation. In PMOP, SIRT1, SIRT3, and SIRT6 are primarily affected. Oxidative stress (OS) is a crucial factor in PMOP, as it generates excessive reactive oxygen species (ROS) that exacerbate PMOP. There is a certain interplay between SIRTs and OS. The reduced activity of SIRTs leads to intensified OS and the excessive accumulation of ROS. In return, ROS suppresses the AMPK signaling pathway and the synthesis of NAD+, which consequently diminishes the function of SIRTs. Natural SIRT activators and natural antioxidants, which are characterized by high safety, convenience, and minimal side effects, represent a potential therapeutic strategy for PMOP. This study aims to investigate the mechanisms of SIRTs and OS in PMOP and summarize potential therapeutic strategies to assist in the improvement of PMOP.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108454/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lysine Carboxymethyl Cysteinate, as a Topical Glutathione Precursor, Protects Against Oxidative Stress and UVB Radiation-Induced Skin Damage.","authors":"Ping Gao, Xue Xiao, Xiao Cui, Hong Zhang, Xuelan Gu","doi":"10.3390/antiox14050606","DOIUrl":"10.3390/antiox14050606","url":null,"abstract":"<p><p>Lysine carboxymethyl cysteinate (LCC) is a synthetic substance obtained via lysine salification of S-carboxymethyl-cysteine. LCC has emerged as a promising glutathione (GSH) precursor. In this study, we sought to determine whether LCC could boost GSH levels and protect skin against oxidative stress. Experiments utilizing primary human keratinocytes and skin tissue samples revealed that LCC significantly increased endogenous GSH levels. LCC was able to pass through the stratum corneum and reach deep into the epidermis, where it enhanced the production of key metabolites involved in GSH biosynthesis. Then, the efficacy of LCC on skin protection was explored. LCC demonstrated protective effects by shielding keratinocytes from blue-light-induced oxidative stress and preventing ultraviolet B (UVB)-induced barrier disruption and pigmentation in a pigmented living skin equivalent (pLSE) model. In addition to its antioxidant properties, LCC also reduced the production of inflammatory mediators. Together, these findings underscore the multifaceted role of LCC in bolstering the natural antioxidant defenses of skin and preventing the accumulation of irreversible damage from the environment, thereby positioning it as a promising candidate for advancing skin health.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endosomal H₂O₂ Molecules Act as Signaling Mediators in Akt/PKB Activation.","authors":"Sujin Park, Chaewon Kim, Sukyeong Heo, Dongmin Kang","doi":"10.3390/antiox14050594","DOIUrl":"10.3390/antiox14050594","url":null,"abstract":"<p><p>Receptor-mediated endocytosis (RME) is a commonly recognized receptor internalization process of receptor degradation or recycling. However, recent studies have supported that RME is closely related to signal propagation and amplification from the plasma membrane to the cytosol. Few studies have elucidated the role of H₂O₂, a mild oxidant among reactive oxygen species (ROS) in RME and second messenger of signal propagation. In the present study, we investigated the regulatory function of H₂O₂ in early endosomes during signaling throughout receptor-mediated endocytosis. In mammalian cells with a physiological amount of H₂O₂ generated during epidermal growth factor (EGF) activation, fluorescence imaging showed that the levels of two activating phosphorylations on Ser⁴⁷³ and Thr³⁰⁸ of Akt were transiently increased in the plasma membrane, but the predominant p-Akt on Ser⁴⁷³ appeared in early endosomes. To examine the role of endosomal H₂O₂ molecules as signaling mediators of Akt activation in endosomes, we modulated endosomal H₂O₂ through the ectopic expression of an endosomal-targeting catalase (Cat-Endo). The forced removal of endosomal H₂O₂ inhibited the Akt phosphorylation on Ser⁴⁷³ but not on Thr³⁰⁸. The levels of mSIN and rictor, two components of mTORC2 that work as a kinase in Akt phosphorylation on Ser⁴⁷³, were also selectively diminished in the early endosomes of Cat-Endo-expressing cells. We also observed a decrease in the endosomal level of the adaptor protein containing the PH domain, the PTB domain, and the Leucine zipper motif 1 (APPL1) protein, which is an effector of Rab5 and key player in the assembly of signaling complexes regulating the Akt pathway in Cat-Endo-expressing cells compared with those in normal cells. Therefore, the H₂O₂-dependent recruitment of the APPL1 adaptor protein into endosomes was required for full Akt activation. We proposed that endosomal H₂O₂ is a promoter of Akt signaling.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blood Progenitor Cell Mobilization Driven by TWEAK Promotes Neovascularization and Reduces Brain Damage in a Rat Model of Intracerebral Hemorrhage.","authors":"Daniel Romaus-Sanjurjo, Esteban López-Arias, Cristina Rodríguez, Pablo Hervella, Mariña Rodríguez-Arrizabalaga, Manuel Debasa-Mouce, Juan Manuel Pías-Peleteiro, Ramón Iglesias-Rey, Pablo Aguiar, Ángeles Almeida, José Castillo, Alberto Ouro, Tomás Sobrino","doi":"10.3390/antiox14050601","DOIUrl":"10.3390/antiox14050601","url":null,"abstract":"<p><p>Non-traumatic intracerebral hemorrhage (ICH) is one of the most devastating and disabling forms of stroke; however, there are no effective pharmacological therapies available following the insult. Angiogenesis appears as a key step to overcoming the damage and promoting functional recovery. In this context, endothelial progenitor cells (EPCs) mobilization improves oxidative stress and promotes neovascularization, which has been linked to beneficial outcomes following both ischemic and hemorrhagic stroke. The TNF-like weak inducer of apoptosis (TWEAK), binding to its receptor Fn14, has been suggested as an inducer of EPCs differentiation, viability and migration to the injury site in a model of myocardial infarction. Here, we have performed a proof-of-concept preclinical study in a rat model of ICH where we report that a 50 μg/kg dose of rat recombinant TWEAK (rTWEAK) promotes blood progenitor cells mobilization, mainly EPCs. As soon as 72 h post-injury, brain neovascularization, and, importantly, long-term hematoma reduction and improved functional recovery is reported. In contrast, a higher dose of 150 μg/kg blocked those beneficial outcomes. Therefore, a low dose of rTWEAK treatment promotes neovascularization and reduces brain damage in a rat model of ICH. Further clinical studies will be needed to demonstrate if rTWEAK could represent a new strategy to promote recovery following ICH.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oleanolic Acid: A Promising Antioxidant-Sources, Mechanisms of Action, Therapeutic Potential, and Enhancement of Bioactivity.","authors":"Andrzej Günther, Barbara Bednarczyk-Cwynar","doi":"10.3390/antiox14050598","DOIUrl":"10.3390/antiox14050598","url":null,"abstract":"<p><p>This review discusses the antioxidant potential of oleanolic acid, a triterpene compound present in many medicinal and edible plants. The authors analyze various studies that confirm numerous pharmacological properties of this compound, such as its anticancer, antidiabetic, neuroprotective, osteoprotective, anti-obesity, and anti-inflammatory effects. OA, as a natural antioxidant, plays an important role in neutralizing reactive oxygen species, which contribute to the oxidative stress that is responsible for the development of many diseases, including cancer and cardiovascular and neurodegenerative diseases. This article also presents natural sources of OA, including grapes, olives, and apples, and discusses the mechanisms of its antioxidant action, including the inhibition of lipid peroxidation and the modulation of signaling pathways related to inflammatory processes. In addition, there are research results that indicate the therapeutic benefits of OA in the treatment of diabetes and neurodegenerative diseases, as well as its potential to protect the heart, liver, and kidneys from oxidative damage. In conclusion, OA has potent antioxidant properties that can be used in the prevention and treatment of many diseases related to oxidative stress. This article also presents the possibility of increasing the bioavailability of OA through the use of nanoparticle and liposome technology.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral Sulforaphane Intervention Protects Against Diabetic Cardiomyopathy in db/db Mice: Focus on Cardiac Lipotoxicity and Substrate Metabolism.","authors":"Pan Wang, Ziling Wang, Xinyuan Jin, Mengdi Zhang, Mengfan Shen, Dan Li","doi":"10.3390/antiox14050603","DOIUrl":"10.3390/antiox14050603","url":null,"abstract":"<p><p>The protective effect of cruciferae-derived sulforaphane (SFN) on diabetic cardiomyopathy (DCM) has garnered increasing attention. However, no studies have specifically explored its mechanistic involvement in cardiac substrate metabolism and mitochondrial function. To address this gap, Type 2 diabetes mellitus (T2DM) db/db mice were orally gavaged with vehicle or 10 mg/kg body weight SFN every other day for 16 weeks, with vehicle-treated wild-type mice as controls. SFN intervention (SFN-I) alleviated hyperglycemia, dyslipidemia, HOMA-IR, serum MDA levels, and liver inflammation. Furthermore, SFN-I improved the lipotoxicity-related phenotype of T2DM cardiomyopathy, manifested as attenuation of diastolic dysfunction, cardiac injury, fibrosis, lipid accumulation and peroxidation, ROS generation, and decreased mitochondrial complex I and II activities and ATP content, despite having no effect on ceramide abnormalities. Protein expression data revealed that the model mice exhibited upregulated cardiac CD36, H-FABP, FATP4, CPT1B, PPARα, and PDK4 but downregulated GLUT4, with unchanged MPC1 and MPC2. Notably, SFN-I significantly attenuated the increase in CD36, H-FABP, CPT1B, and PPARα. These results suggest that chronic oral SFN-I protects against DCM by mitigating overall metabolic dysregulation and inhibiting cardiolipotoxicity. The latter might involve controlling cardiac fatty acid metabolism and improving mitochondrial function, rather than promoting glucose metabolism.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective Effects of Lotus Seedpod Extract on Hepatic Lipid and Glucose Metabolism via AMPK-Associated Mechanisms in a Mouse Model of Metabolic Syndrome and Oleic Acid-Induced HepG2 Cells.","authors":"Hui-Hsuan Lin, Pei-Rong Yu, Chiao-Yun Tseng, Ming-Shih Lee, Jing-Hsien Chen","doi":"10.3390/antiox14050595","DOIUrl":"10.3390/antiox14050595","url":null,"abstract":"<p><p>Metabolic syndrome (MetS) poses considerable toxicological risks due to its association with an increased likelihood of metabolic dysfunction-associated steatotic liver disease (MASLD), and is characterized by hypertension, hyperglycemia, dyslipidemia, and obesity. This study aimed to investigate the therapeutic potential of flavonoid-rich lotus seedpod extract (LSE) in alleviating MetS and MASLD-related hepatic disturbances. In vivo, mice subjected to a high-fat diet (HFD) and streptozotocin (STZ) injection were supplemented with LSE or simvastatin for 6 weeks. Obesity indicators included body weight and epididymal fat, while insulin resistance was measured by fasting serum glucose, serum insulin, homeostasis model assessment-insulin resistance index (HOMA-IR), and oral glucose tolerance (OGTT). Also, the levels of serum lipid profiles and blood pressure were evaluated. Adipokines, proinflammatory cytokines, liver fat droplets, and peri-portal fibrosis were analyzed to clarify the mechanism of MetS. LSE significantly reduced the HFD/STZ-induced MetS markers better than simvastatin, as demonstrated by hypoglycemic, hypolipidemic, antioxidant, and anti-inflammatory effects. In vitro, LSE improved oleic acid (OA)-triggered phenotypes of MASLD in hepatocyte HepG2 cells by reducing lipid accumulation and enhancing cell viability. This effect might be mediated through proteins involved in lipogenesis that are downregulated by adenosine monophosphate-activated protein kinase (AMPK). In addition, LSE reduced reactive oxygen species (ROS) generation and glycogen levels, as demonstrated by enhancing insulin signaling involving reducing insulin receptor substrate-1 (IRS-1) Ser307 phosphorylation and increasing glycogen synthase kinase 3 beta (GSK3β) and protein kinase B (PKB) expression. These benefits were dependent on AMPK activation, as confirmed by the AMPK inhibitor compound C. These results indicate that LSE exhibits protective effects against MetS-caused toxicological disturbances in hepatic carbohydrate and lipid metabolism, potentially contributing to its efficacy in preventing MASLD or MetS.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108490/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Drug Resistance in Cancer: Dimethoxycurcumin as a Functional Antioxidant Targeting ABCC3.","authors":"Jochem Nelen, Valeria Naponelli, José Manuel Villalgordo-Soto, Marco Falasca, Horacio Pérez-Sánchez","doi":"10.3390/antiox14050599","DOIUrl":"10.3390/antiox14050599","url":null,"abstract":"<p><p>The development of new anticancer therapies remains challenging due to tumor heterogeneity and the frequent emergence of multidrug resistance (MDR). Natural products have garnered increasing attention as alternative or complementary therapeutic agents due to their bioactivity and reduced toxicity. Polyphenols, particularly curcumin and its derivatives, have shown promise in modulating signaling pathways, enhancing chemosensitivity, and overcoming drug resistance. The anticancer potential of dimethoxycurcumin, a chemically modified curcumin derivative identified through consensus fingerprint similarity screening, was investigated for its potential to inhibit ABCC3 (MRP3)-a member of the ATP-binding cassette (ABC) transporter family implicated in drug efflux, tumor cell survival, and resistance. In vitro experiments demonstrated that dimethoxycurcumin significantly reduced cancer cell viability and colony formation, indicating a strong inhibitory effect on ABCC3 function. These results suggest that dimethoxycurcumin may sensitize cancer cells to chemotherapy by targeting resistance pathways. The data presented contribute to the growing body of evidence suggesting that bioactive plant-derived compounds, including chemically modified derivatives, may hold therapeutic potential in oncology by modulating multidrug resistance pathways. Targeting ABC transporters with natural compound derivatives could offer a promising strategy for developing more effective and less toxic anticancer therapies.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Class III Peroxidase Gene Family in <i>Populus simonii</i>: Genome-Wide Identification, Classification, Gene Expression and Functional Analysis.","authors":"Lu Han, Yishuang Ren, Xinru Bi, Guowei Yao, Jinwang Zhang, Hongtao Yuan, Xiaoyu Xie, Junbo Chen, Yunchang Zhang, Sitong Du, Wanying Chen, Kewei Cai, Xiyang Zhao","doi":"10.3390/antiox14050602","DOIUrl":"10.3390/antiox14050602","url":null,"abstract":"<p><p>Class III peroxidases are plant-specific enzymes that play indispensable roles in catalyzing oxidative-reductive reactions, which are integral to numerous biochemical processes in plants. In this study, we identified 69 members of the class III peroxidase (<i>POD</i>) gene family in the <i>Populus simonii</i> genome and classified them into four subfamilies based on phylogenetic analysis. Chromosomal localization revealed that these <i>PsPOD</i> genes are unevenly distributed across 19 chromosomes, with chromosomes 3 and 7 harboring the highest densities. Conserved domain and motif analyses demonstrated that all <i>PsPOD</i> proteins contain the characteristic peroxidase domain and share highly conserved motif structures. Cis-acting element analysis of promoter regions revealed the presence of numerous regulatory elements associated with light responsiveness, phytohormone signaling, stress responses, and plant growth and development. Transcriptome data showed that the expression of <i>PsPOD</i> genes varies significantly across different tissues and organs and under various stress conditions, suggesting their involvement in both developmental processes and abiotic stress responses. These findings were further validated by qRT-PCR analysis of selected <i>PsPOD</i> genes. Notably, <i>PsPOD45</i>, <i>PsPOD69</i>, <i>PsPOD33</i>, and <i>PsPOD64</i> were identified as central hub genes in the protein-protein interaction network, making them promising candidates for further functional characterization. Overall, this study provides a comprehensive overview of the <i>PsPOD</i> gene family in <i>P. simonii</i>, laying a solid foundation for future functional studies and offering valuable insights for comparative research in other plant species.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}