Biochimica et biophysica acta. General subjects最新文献

{"title":"Coupling of muscarinic receptors to protein kinase C underlies a feedback regulation of cell responsiveness to acetylcholine","authors":"Ekaterina A. Dymova,&nbsp;Olga A. Rogachevskaja,&nbsp;Vladislav V. Sokolov,&nbsp;Elizaveta Е. Kopylova,&nbsp;Natalia V. Kabanova,&nbsp;Stanislav S. Kolesnikov","doi":"10.1016/j.bbagen.2025.130844","DOIUrl":"10.1016/j.bbagen.2025.130844","url":null,"abstract":"<div><div>Acetylcholine (ACh)-induced Ca²⁺ signaling was analyzed in HEK-293 (WT-HEK) cells and their derivatives, IP3R1-HEK, IP3R2-HEK, and IP3R3-HEK with a single functional IP₃ receptor isoform, IP₃R1, IP₃R2, or IP₃R3, respectively. The initial stimulation of WT-HEK cells triggered a prolonged feedback process that diminished their responsiveness to ACh. Inhibition of protein kinase C (PKC) with Gö 6983 or calphostin C prevented the decline of ACh responsivity, indicating that PKC was involved. Using IP3R1-HEK, IP3R2-HEK, and IP3R3-HEK cells, it was shown that PKC was capable of regulating Ca²⁺ release through each IP₃R isoform. While in control, IP₃ uncaging triggered Ca²⁺ transients in ∼15 % of cells loaded with caged-Ins(145)P3/PM, PKC inhibition enlarged this fraction nearly twofold. These observations suggested that in ACh transduction machinery, PKC targeted primarily IP₃-driven Ca²⁺ release. ADP and 5-HT triggered Ca²⁺ transients in WT-HEK cells and CHO cells expressing endogenous P2Y and recombinant 5HT2C receptors, respectively. The responsiveness of WT-HEK cells to ADP and CHO cells to 5-HT applied serially declined after the initial cell stimulation but PKC inhibition precluded this phenomenon almost completely. The coupling of GPCRs to PKC in living cells, muscarinic and P2Y receptors in WT-HEK cells and 5HT2C receptors in CHO cells, was demonstrated for the first time using real-time fluorescence imaging and sapphireCKAR, a genetically encoded sensor of PKC activity. Altogether, our findings suggest that a PKC-based feedback regulation of agonist-induced Ca²⁺ release might be a common attribute of transduction of various agonists involving GPCRs coupled to the phosphoinositide cascade.</div></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 10","pages":"Article 130844"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717301","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}

{"title":"IRF1 transcriptionally activates ALOX15B to enhance ferroptosis sensitivity in triple-negative breast cancer","authors":"Wei Peng,&nbsp;Yi Xie,&nbsp;Bofeng Duan,&nbsp;Fuyong Qian,&nbsp;Zhifeng Fan,&nbsp;Wei Zheng","doi":"10.1016/j.bbagen.2025.130846","DOIUrl":"10.1016/j.bbagen.2025.130846","url":null,"abstract":"<div><div>This study focused on the transcriptional activation of arachidonate 15-lipoxygenase type B (ALOX15B) by interferon regulatory factor 1 (IRF1) to promote ferroptosis in triple-negative breast cancer (TNBC) cells. In this study, TNBC and adjacent non-cancerous tissues were collected to detect ALOX15B expression. Functional studies were conducted by overexpressing or knocking down ALOX15B in TNBC cells treated with erastin (a ferroptosis inducer). The role of IRF1 as a potential transcriptional regulator of ALOX15B was explored using bioinformatics tools, dual-luciferase reporter gene assays, electrophoretic mobility shift assays (EMSA), and chromatin immunoprecipitation (ChIP) followed by quantitative polymerase chain reaction (qPCR). Our results revealed that ALOX15B expression was significantly lower in TNBC tissues compared to adjacent non-cancerous tissues. Functionally, ALOX15B overexpression inhibited ferroptosis-related proteins SLC7A11 and GPX4, decreased cell viability and glutathione levels, and increased malondialdehyde levels, reactive oxygen species levels, and lipid oxidation. Conversely, knocking down ALOX15B had the opposite effect. Bioinformatics analysis predicted IRF1 as a potential transcriptional regulator of ALOX15B, which was confirmed using dual-luciferase reporter gene assays, EMSA, and ChIP-qPCR. IRF1 overexpression increased ALOX15B expression and promoted ferroptosis in TNBC cells, while IRF1 knockdown had the opposite effect. Importantly, knocking down IRF1 and overexpressing ALOX15B simultaneously demonstrated that IRF1 enhanced TNBC cell ferroptosis sensitivity by promoting ALOX15B expression. Collectively, our study suggests that IRF1 transcriptionally activates ALOX15B to enhance ferroptosis sensitivity in TNBC cells. These findings provide new insights into the molecular mechanisms underlying TNBC progression and suggest potential therapeutic targets for TNBC treatment.</div></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 10","pages":"Article 130846"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144757771","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}

{"title":"Nitrosative stress affects mitochondrial respiratory chain complex II and complex IV assemblies in Saccharomyces cerevisiae: S-nitrosylation of complex II","authors":"Sanchita Biswas ,&nbsp;Ayantika Sengupta ,&nbsp;Shubhojit Das ,&nbsp;Chirandeep Dey ,&nbsp;Rajib Sengupta ,&nbsp;Alok Ghosh ,&nbsp;Sanjay Ghosh","doi":"10.1016/j.bbagen.2025.130845","DOIUrl":"10.1016/j.bbagen.2025.130845","url":null,"abstract":"<div><div>The elevated level of nitric oxide (NO) and reactive nitrogen species (RNS) induce nitrosative stress in cells and inhibit mitochondrial respiration. Reports showed that RNS rapidly inactivate complex I, followed by inhibition of complex II, III and IV in isolated mitochondria. However, the mechanism(s) by which NO and RNS inhibit these complexes still unclear. In this study facultative anaerobic yeast <em>Saccharomyces cerevisiae</em> has been used for investigating mitochondrial respiratory dysfunction under nitrosative stress, as four out of five mitochondrial oxidative phosphorylation complexes i.e. complexes II, III, IV and V are structurally conserved from yeast to human. Using microbiological growth assays, we showed that <em>S. cerevisiae</em> wild type W3O3 cells treated with graded concentration of sodium nitroprusside (SNP) and S-Nitrosoglutathione (GSNO) induce nitrosative stress, and cell growth was severely compromised under the respiratory proficient rich glycerol-ethanol media. Both the whole cell and the mitochondrial oxygen consumption rates were also significantly compromised under nitrosative stress. Surprisingly, mitochondrial respiratory chain complex II succinate dehydrogenase (SDH) of <em>S. cerevisiae</em> was found S-nitrosylated and therefore inactivated under nitrosative stress. Endogenous RNS produced by S-nitrosoglutathione reductase mutant cells of <em>S. cerevisiae</em> also showed increased S-nitrosylation of SDH. Complex III and IV activities were irreversibly inhibited in <em>S. cerevisiae</em> under nitrosative stress. Interestingly, protein tyrosine nitration was also enhanced in mitochondria in a dose dependent manner upon SNP treatment. Reduced expressions of both Sdh2 (succinate dehydrogenase subunit-2) and Cox2 (mitochondrial complex IV subunit) were observed at the transcription and translation level in <em>S. cerevisiae</em> under nitrosative stress. Blue Native-PAGE followed by Western blotting analysis, further revealed significantly reduced native complex II and the complex III and IV containing super-complexes assemblies in consequences of nitrosative stress in <em>S. cerevisiae</em>. Henceforth, the present in vivo study provides for the first-time novel information on the modification of mitochondrial complexes under nitrosative stress which in turn regulates the mitochondrial respiratory chain complexes assembly in <em>S. cerevisiae</em>.</div></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 10","pages":"Article 130845"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764457","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}

{"title":"Pharmacological role of MLN4924 in cisplatin-induced acute kidney injury","authors":"Feng Chen ,&nbsp;Ayinigaer Yusufu ,&nbsp;Gang Li ,&nbsp;Xueyun Gao ,&nbsp;Danqin Lu ,&nbsp;Xiaoyan Wu ,&nbsp;Lihua Ni","doi":"10.1016/j.bbagen.2025.130842","DOIUrl":"10.1016/j.bbagen.2025.130842","url":null,"abstract":"<div><h3>Background</h3><div>Cisplatin-induced acute kidney injury (Cis-AKI) is a major complication that limits the clinical use of cisplatin, largely due to its cytotoxic effects on renal tubular epithelial cells. Recent studies have shown that MLN4924, a NEDD8-activating enzyme inhibitor, can modulate key cellular processes such as apoptosis, autophagy, and DNA damage repair. However, its precise role and regulatory mechanisms in the context of Cis-AKI remain largely undefined.</div></div><div><h3>Purpose</h3><div>This study aimed to elucidate the renoprotective mechanisms of MLN4924 in Cis-AKI.</div></div><div><h3>Materials and methods</h3><div>A cisplatin-induced nephrotoxicity mouse model and a human renal tubular epithelial (HK−2) damage cellular model were established. Kidney injury was evaluated by histopathology and RNA-sequencing. To explore whether MLN4924 alleviates Cis-AKI via modulation of the p53 and MAPK pathways, we analyzed pathway-specific regulatory changes in response to MLN4924 treatment.</div></div><div><h3>Results</h3><div>Compared to the group exposed to cisplatin, MLN4924 mitigated the pathological alterations and reduced the expression of molecules associated with renal injury. RNA-sequencing analysis indicated that the p53 and MAPK signaling pathways were inhibited by MLN4924 treatment compared to the cisplatin-exposed group. Moreover, silencing p53 or p38 exacerbates the renal protection conferred by MLN4924 in cisplatin-treated HK-2 cells, while their activation abolishes this effect. Mechanically, p38 activity promoted p53-dependent nephrotoxicity by increasing p53 expression.</div></div><div><h3>Conclusions</h3><div>MLN4924 exhibits a protective effect against Cis-AKI, as evidenced by inhibition of p53 and MAPK signaling pathways. These results suggest that MLN4924 holds potential as an adjuvant therapeutic agent in the treatment of kidney diseases associated with chemotherapy.</div></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 10","pages":"Article 130842"},"PeriodicalIF":2.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144633598","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}

{"title":"Editorial: Nondomain biopolymers – Flexible molecular strategies for diverse biological processes","authors":"Shinichi Nakagawa","doi":"10.1016/j.bbagen.2025.130847","DOIUrl":"10.1016/j.bbagen.2025.130847","url":null,"abstract":"","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 10","pages":"Article 130847"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144803357","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}

{"title":"Gamma radiation assisted green synthesis of spirulina-reduced graphene oxide and its anti-inflammatory effect against renal injury induced by gamma irradiation via IRE1α -TRAF2 pathway","authors":"M.M. Atta ,&nbsp;Marwa A. Mohamed ,&nbsp;Aliaa Mazhar ,&nbsp;Fatma Y. Abdou ,&nbsp;E.O. Taha ,&nbsp;Mahmoud E. Habieb","doi":"10.1016/j.bbagen.2025.130840","DOIUrl":"10.1016/j.bbagen.2025.130840","url":null,"abstract":"<div><h3>Background</h3><div>Combining gamma rays with natural antioxidants leads to the formation of reduced graphene oxide (RGO) biocomposites from graphene oxide (GO) in a way that is both incredibly safe and environmentally friendly, unlocking new possibilities for medical use.</div></div><div><h3>Methods</h3><div>In the present study, spirulina-reduced graphene oxide nanocomposites (SRGOs) were fabricated by gamma rays as a one-step and straightforward technique.The loading and reduction of graphene oxide in the presence of different spirulina ratios (25, 50, 100, and 200 wt%) under gamma irradiation were verified by diverse characterization apparatuses, including XRD, FTIR, HRTEM, and XPS. Moreover, in vivo studies are conducted to investigate the anti-inflammatory properties of the selected SRGO nanocomposite in preventing kidney injury caused by gamma irradiation.</div></div><div><h3>Results</h3><div>SRGO amended the renal levels of interleukin-6 (IL-6), IL-8, Inositol requirement enzyme 1α (IRE1α), and TNF receptor-associated factor 2 (TRAF2), the protein expression of NF-κB p65, and the levels of GSH, MDA, serum urea, and creatinine. In the context of oxidative stress and inflammatory biomarkers, the histopathological study results of kidney tissue concurred with those of the molecular biochemical examinations.</div></div><div><h3>Conclusion</h3><div>The findings endorsed SRGO biocomposite as a promising antioxidant, radioprotector, and anti-inflammatory agent in mitigating kidney damage caused by γ-radiation via significant inhibition of the IRE1α-TRAF2 signaling pathway.</div></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 10","pages":"Article 130840"},"PeriodicalIF":2.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144633597","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}

{"title":"MYO9B deficiency promoted head and neck tumor progression through HIF1α/MYC/STAT2 signaling pathway","authors":"Simin Gao ,&nbsp;Xia Gao ,&nbsp;Ning Wang ,&nbsp;Yuping Xie ,&nbsp;Yuedi Tang","doi":"10.1016/j.bbagen.2025.130834","DOIUrl":"10.1016/j.bbagen.2025.130834","url":null,"abstract":"<div><h3>Background</h3><div>Myosin, a protein family primarily involved in muscle contraction and cell movement, plays critical roles in various biological processes. Increasing evidence suggests its implication in tumor development and progression. However, the underlying mechanism remains poorly understood. Our study aimed to explore the role and molecular mechanism of myosin IXB (MYO9B) in head and neck squamous cell carcinoma (HNSC) development.</div></div><div><h3>Methods</h3><div>Utilizing The Cancer Genome Atlas (TCGA) database (<em>n</em> = 24) and analyzing clinical HNSC tissues (n = 24), we investigated the correlation between myosin encoding genes and HNSC progression. Cell proliferation and migration were assessed using CCK8 and Transwell assays to elucidate the tumor suppressive role of MYO9B. Additionally, Western blotting and immunostaining were conducted to evaluate the activation of HIF1α/c-Myc/STAT2 signaling. A 3D Matrigel Primary tumor cell culture model was established to assess the cisplatin resistance of HNSC cells.</div></div><div><h3>Results</h3><div>We found that MYO9B deficiency predicted poor prognosis in HNSC patients. In vitro, inhibiting MYO9B enhanced the proliferative and migratory characteristics of HNSC cell lines. Mechanistically, our study showed that MYO9B deficiency upregulated HIF1α signaling, leading to c-Myc upregulation, which induced stem-like phenotypes in cancer cells and HNSC progression. Furthermore, c-Myc upregulated downstream STAT2 signaling, contributing to cisplatin resistance in HNSC cells. Blocking STAT2 signaling improved cisplatin outcomes in primary MYO9B-high HNSC tissues from patients.</div></div><div><h3>Conclusion</h3><div>Our study highlights the tumor suppressive role of MYO9B through HI1F1α/c-Myc/STAT2 in HNSC, suggesting its potential as a diagnostic indicator and therapeutic target for clinical intervention.</div></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 9","pages":"Article 130834"},"PeriodicalIF":2.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301037","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}

{"title":"Antibiotic-induced mitochondrial dysfunction: Exploring tissue-specific effects on HEI-OC1 cells and peripheral blood mononuclear cells","authors":"Tianshi Liu ,&nbsp;Imen Chamkha ,&nbsp;Eskil Elmér ,&nbsp;Fredrik Sjövall ,&nbsp;Johannes K. Ehinger","doi":"10.1016/j.bbagen.2025.130832","DOIUrl":"10.1016/j.bbagen.2025.130832","url":null,"abstract":"<div><div>Antibiotics are crucial in treating infectious diseases, particularly in intensive care unit patients, but they can lead to side effects such as ototoxicity. A mechanism for this is antibiotics targeting mitochondrial components in eucaryotic cells, due to their resemblance of those in bacteria. Here we investigate how five classes of antibiotics (carbapenems, fluoroquinolones, aminoglycosides, glycopeptides, and oxazolidinones) affect mitochondrial respiratory function, ATP levels, mitochondrial membrane potential and levels of reactive oxygen species in an inner-ear derived epithelial cell line (HEI-OC1) and human primary blood cells (PBMCs) at clinically relevant concentrations.</div><div>Mitochondrial respiration in intact HEI-OC1 cells was suppressed in response to the majority of the tested antibiotics. This effect was lost when the HEI-OC1 cells were permeabilized and substrate supply controlled. Further in these cells, ROS levels were increased and ATP levels reduced. In contrast, no measure of mitochondrial function of PBMCs was affected by any antibiotics at the same concentration. We show that HEI-OC1 cells are sensitive to a broad range of antibiotics, and that the mechanism of toxicity to mitochondrial respiration is upstream of the mitochondrial respiratory chain, with downstream effects on mitochondrial respiration, ATP levels and ROS levels.</div></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 9","pages":"Article 130832"},"PeriodicalIF":2.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293186","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}

{"title":"The polyphenols phloretin and quercetin are potent horseradish peroxidase (HRP) inhibitors","authors":"Ben Faerman ,&nbsp;Olivia Chalifoux ,&nbsp;Marek Michalak ,&nbsp;Luis B. Agellon ,&nbsp;Ryan J. Mailloux","doi":"10.1016/j.bbagen.2025.130833","DOIUrl":"10.1016/j.bbagen.2025.130833","url":null,"abstract":"<div><div>The discovery of horseradish peroxidase (HRP) has been highly advantageous because its unique chemistry can be applied to diagnostic tools, including the detection of oxidative distress markers like hydrogen peroxide (H₂O₂) in various experimental systems. Here, we made the surprising and compelling finding that the flavonoids, phloretin and quercetin, which are usually described in the literature as potent antioxidants, strongly inhibit the activity of HRP. Using the amplex ultrared (AUR) assay, we discovered that phloretin at a concentration as low as 50 μM abolishes the detection of H₂O₂ production by isolated liver mitochondria oxidizing pyruvate and malate. Phloretin also nullified the detection of H₂O₂ produced by liver mitochondria oxidizing succinate or dihydroorotate. Moreover, phloretin at 100 μM completely abolished the direct detection of H₂O₂ by AUR and quenched the detection of purified xanthine oxidase (XO) activity, but did not interfere with dichlorodihydrofluorescein diacetate (H₂-DCFDA) or dihydroethidine (DHE) fluorescent assays. Dose response assays revealed quercetin is a more potent inhibitor for HRP when compared to phloretin. Indeed, quercetin abolished resorufin fluorescence in AUR assays in the nM range whereas phloretin had no effect when detecting H₂O₂ <em>in vitro</em> or when it is formed by isolated liver mitochondria or cultured Huh-7 hepatoma and Mia-PaCa2 cells. Collectively, our findings demonstrate phloretin and quercetin, and potentially other polyphenols, potently interfere with HRP-dependent assays, which have strong implications for designing experiments that interrogate the antioxidant potential of flavonoids. Our results also indicate phloretin and quercetin could be applied as controls for HRP reporter assays.</div></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 9","pages":"Article 130833"},"PeriodicalIF":2.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301038","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}

{"title":"Nitric oxide in plant stress: Rewilding and restoring signaling for enhancing plant growth and development","authors":"Sumreen Amin Shah ,&nbsp;Awdhesh Kumar Mishra ,&nbsp;Abdul Rehaman ,&nbsp;Sumit G. Gandhi ,&nbsp;Arif Tasleem Jan","doi":"10.1016/j.bbagen.2025.130837","DOIUrl":"10.1016/j.bbagen.2025.130837","url":null,"abstract":"<div><div>Plants, represented as a complex system, are continuously exposed to environmental conditions that affect their growth and development, and sometimes their survival. Being sessile, they complete their life cycle under the influence of varied environmental constraints (biotic and abiotic), that adversely affect the produce's quality and productivity. Plants have evolved several defense strategies orchestrated through phytohormones that play a pivotal role in conferring resistance to stress. Nitric oxide (NO), an endogenously produced gaseous hormone, has emerged as a saviour in plant's response to different stresses. It plays an active role in the growth and development of plants, from seed dormancy and germination to growth, differentiation, flowering, fruiting, and ripening, besides affecting key metabolic processes such as photosynthesis. Endogenous production of NO and its interaction with phytohormones across different signaling cascades helps in alleviating the cellular damage caused by free radicals during drought, salinity, and other stresses. It contributes to stress resilience by inducing the synthesis of stress hormones such as ethylene (ET), which help plants to withstand adverse environmental constraints by minimizing the damage caused by different stresses. Exogenous application of NO exerts protective effects against different stresses by breaking seed dormancy and modulating germination, enhancing acquisition of mineral nutrients, photosynthetic functioning, production of antioxidant enzymes capable of neutralizing free radicals, and maintaining membrane integrity. These multifaceted roles of NO underscore its significance in plant stress tolerance. The present study offers valuable insights into NO production methods, involvement in growth and development, and a mechanistic view of its role in alleviating different stresses. In the current scenario, continued research into NO signaling mechanisms and cross-talk with other pathways seems essential for harnessing its potential in developing crops with enhanced resilience to environmental challenges.</div></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 9","pages":"Article 130837"},"PeriodicalIF":2.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144366653","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}