Nitric oxide : biology and chemistry最新文献

{"title":"Role of hydrogen sulfide in dermatological diseases","authors":"","doi":"10.1016/j.niox.2024.07.001","DOIUrl":"10.1016/j.niox.2024.07.001","url":null,"abstract":"<div><p>Hydrogen sulfide (H₂S), together with carbon monoxide (CO) and nitric oxide (NO), is recognized as a vital gasotransmitter. H₂S is biosynthesized by enzymatic pathways in the skin and exerts significant physiological effects on a variety of biological processes, such as apoptosis, modulation of inflammation, cellular proliferation, and regulation of vasodilation. As a major health problem, dermatological diseases affect a large proportion of the population every day. It is urgent to design and develop effective drugs to deal with dermatological diseases. Dermatological diseases can arise from a multitude of etiologies, including neoplastic growth, infectious agents, and inflammatory processes. The abnormal metabolism of H₂S is associated with many dermatological diseases, such as melanoma, fibrotic diseases, and psoriasis, suggesting its therapeutic potential in the treatment of these diseases. In addition, therapies based on H₂S donors are being developed to treat some of these conditions. In the review, we discuss recent advances in the function of H₂S in normal skin, the role of altering H₂S metabolism in dermatological diseases, and the therapeutic potential of diverse H₂S donors for the treatment of dermatological diseases.</p></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"150 ","pages":"Pages 18-26"},"PeriodicalIF":3.2,"publicationDate":"2024-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141545117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Carbon monoxide-releasing Vehicle CO@TPyP-FeMOFs modulating macrophages phenotype in inflammatory wound healing","authors":"Yixian Mu ,&nbsp;Xinlei Yang ,&nbsp;Yinhong Xie ,&nbsp;Jie Luo ,&nbsp;Sui Wu ,&nbsp;JinMing Yang ,&nbsp;Wei Zhao ,&nbsp;Junying Chen ,&nbsp;Yajun Weng","doi":"10.1016/j.niox.2024.06.005","DOIUrl":"10.1016/j.niox.2024.06.005","url":null,"abstract":"<div><p>Healing of chronic wounds has been critically limited by prolonged inflammation. Carbon monoxide (CO) is a biologically active molecule with high potential based on its efficacy in modulating inflammation, promoting wound healing and tissue remodeling. Strategies to use CO as a gaseous drug to chronic wounds have emerged, but controlling the sustained release of CO at the wound site remains a major challenge. In this work, a porphyrin-Fe based metal organic frameworks, TPyP-FeMOFs was prepared. The synthesized TPyP-FeMOFs was high-temperature vacuum activated (AcTPyP-FeMOFs) and AcTPyP-FeMOFs had a relatively high Fe (II) content. CO sorption isotherms showed that AcTPyP-FeMOFs chemisorbed CO and thus CO release was sustained and prolonged. In vitro evaluation results showed that CO@TPyP-FeMOFs reduced the inflammatory level of lipopolysaccharide (LPS) activated macrophages, polarized macrophages to M2 anti-inflammatory phenotype, and promoted the proliferation of fibroblasts by altering the pathological microenvironment. In vivo study confirmed CO@TPyP-FeMOFs promoted healing in a LPS model of delayed cutaneous wound repair and reduced macrophages and neutrophils recruitment. Both in vitro and in vivo studies verified that CO@TPyP-FeMOFs acted on macrophages by modulating phenotype and inflammatory factor expression. Thus, CO release targeting macrophages and pathological microenvironment modulation presented a promising strategy for wound healing.</p></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"149 ","pages":"Pages 49-59"},"PeriodicalIF":3.9,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141420095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium thiosulfate: A donor or carrier signaling molecule for hydrogen sulfide?","authors":"Si-Miao Tang ,&nbsp;Guo-Zhong Lu ,&nbsp;Xiao-Yong Lei ,&nbsp;Xiao-Yan Yang ,&nbsp;Guo-Tao Tang ,&nbsp;Jia Yu ,&nbsp;Zhi-Zhong Xie","doi":"10.1016/j.niox.2024.06.004","DOIUrl":"10.1016/j.niox.2024.06.004","url":null,"abstract":"<div><p>Sodium thiosulfate has been used for decades in the treatment of calciphylaxis and cyanide detoxification, and has recently shown initial therapeutic promise in critical diseases such as neuronal ischemia, diabetes mellitus, heart failure and acute lung injury. However, the precise mechanism of sodium thiosulfate remains incompletely defined and sometimes contradictory. Although sodium thiosulfate has been widely accepted as a donor of hydrogen sulfide (H₂S), emerging findings suggest that it is the executive signaling molecule for H₂S and that its effects may not be dependent on H₂S. This article presents an overview of the current understanding of sodium thiosulfate, including its synthesis, biological characteristics, and clinical applications of sodium thiosulfate, as well as the underlying mechanisms <em>in vivo</em>. We also discussed the interplay of sodium thiosulfate and H₂S. Our review highlights sodium thiosulfate as a key player in sulfide signaling with the broad clinical potential for the future.</p></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"149 ","pages":"Pages 67-74"},"PeriodicalIF":3.2,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141427357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of continuous low-dose and high-dose burst of inhaled nitric oxide in spontaneously breathing COVID-19 patients: A randomized controlled trial","authors":"Nikolay O. Kamenshchikov ,&nbsp;Bijan Safaee Fakhr ,&nbsp;Igor V. Kravchenko ,&nbsp;Andrey Yu Dish ,&nbsp;Yuri K. Podoksenov ,&nbsp;Boris N. Kozlov ,&nbsp;Tatiana P. Kalashnikova ,&nbsp;Mark A. Tyo ,&nbsp;Nina D. Anfinogenova ,&nbsp;Alla A. Boshchenko ,&nbsp;Lorenzo Berra","doi":"10.1016/j.niox.2024.06.003","DOIUrl":"10.1016/j.niox.2024.06.003","url":null,"abstract":"<div><h3>Background</h3><p>Inhaled nitric oxide (iNO) showed to improve oxygenation at low doses by reducing intrapulmonary shunt and to display antiviral properties at high doses. To assess the safety and potential benefits, we designed an exploratory clinical trial comparing low-dose with intermittent high-dose iNO to only intermittent high-dose iNO in hypoxemic COVID-19 patients.</p></div><div><h3>Methods</h3><p>In this single-center interventional non-inferiority randomized trial (<span>ClinicalTrials.gov</span><svg><path></path></svg>, NCT04476992), twenty oxygen-dependent COVID-19 patients were randomly assigned to the high-dose (200 ppm for 30 min) + continuous low-dose (20 ppm) iNO group (iNO_200/20) or the high-dose iNO group (iNO₂₀₀). Methemoglobinemia (MetHb) assessed 48 h after iNO initiation was the primary endpoint. Reverse-transcription polymerase chain reaction for SARS-CoV-2, inflammatory markers during hospitalization, and heart ultrasounds during the iNO₂₀₀ treatments were evaluated.</p></div><div><h3>Results</h3><p>MetHb difference between iNO groups remained within the non-inferiority limit of 3 %, indicating comparable treatments despite being statistically different (p-value&lt;0.01). Both groups presented similar SpO₂/FiO₂ ratio at 48 h (iNO₂₀₀ vs. iNO_200/20 341[334–356] vs. 359 [331–380], respectively, p-value = 0.436). Both groups showed the same time to SARS-CoV-2 negativization, hospital length of stay, and recovery time. iNO-treated patients showed quicker SARS-CoV-2 negativization compared to a similar group of non-iNO patients (HR 2.57, 95%CI 1.04–6.33). During the 228 treatments, iNO₂₀₀ and iNO_200/20 groups were comparable for safety, hemodynamic stability, and respiratory function improvement.</p></div><div><h3>Conclusions</h3><p>iNO_200/20 and iNO₂₀₀ are equally safe in non-intubated patients with COVID-19-induced respiratory failure with regards to MetHb and NO₂. Larger studies should investigate whether iNO_200/20 leads to better outcomes compared to non-iNO treated patients.</p></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"149 ","pages":"Pages 41-48"},"PeriodicalIF":3.9,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141331519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adipocyte-specific Nrf2 deletion negates nitro-oleic acid benefits on glucose tolerance in diet-induced obesity","authors":"D.V. Chartoumpekis ,&nbsp;I. Chen ,&nbsp;S.R. Salvatore ,&nbsp;F.J. Schopfer ,&nbsp;B.A. Freeman ,&nbsp;N.K.H. Khoo","doi":"10.1016/j.niox.2024.06.002","DOIUrl":"10.1016/j.niox.2024.06.002","url":null,"abstract":"<div><p>Obesity is commonly linked with white adipose tissue (WAT) dysfunction, setting off inflammation and oxidative stress, both key contributors to the cardiometabolic complications associated with obesity. To improve metabolic and cardiovascular health, countering these inflammatory and oxidative signaling processes is crucial. Offering potential in this context, the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) by nitro-fatty acids (NO₂-FA) promote diverse anti-inflammatory signaling and counteract oxidative stress. Additionally, we previously highlighted that nitro-oleic acid (NO₂-OA) preferentially accumulates in WAT and provides protection against already established high fat diet (HFD)-mediated impaired glucose tolerance. The precise mechanism accounting for these protective effects remained largely unexplored until now. Herein, we reveal that protective effects of improved glucose tolerance by NO₂-OA is absent when Nrf2 is specifically ablated in adipocytes (ANKO mice). NO₂-OA treatment did not alter body weight between ANKO and littermate controls (Nrf2^fl/fl) mice on both the HFD and low-fat diet (LFD). As expected, at day 76 (before NO₂-OA treatment) and notably at day 125 (daily treatment of 15 mg/kg NO₂-OA for 48 days), both HFD-fed Nrf2^fl/fl and ANKO mice exhibited increased fat mass and reduced lean mass compared to LFD controls. However, throughout the NO₂-OA treatment, no distinction was observed between Nrf2^fl/fl and ANKO in the HFD-fed mice as well as in the Nrf2^fl/fl mice fed a LFD. Glucose tolerance tests revealed impaired glucose tolerance in HFD-fed Nrf2^fl/fl and ANKO compared to LFD-fed Nrf2^fl/fl mice. Notably, NO₂-OA treatment improved glucose tolerance in HFD-fed Nrf2^fl/fl but did not yield the same improvement in ANKO mice at days 15, 30, and 55 of treatment. Unraveling the pathways linked to NO₂-OA's protective effects in obesity-mediated impairment in glucose tolerance is pivotal within the realm of precision medicine, crucially propelling future applications and refining novel drug-based strategies.</p></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"149 ","pages":"Pages 75-84"},"PeriodicalIF":3.2,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1089860324000776/pdfft?md5=ad2f79fdb7ebaa2e2587ac6ddb7537ad&pid=1-s2.0-S1089860324000776-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141327717","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}

{"title":"An observational analysis on the influence of parental allergic rhinitis, asthma and smoking on exhaled nitric oxide in offspring","authors":"S. Zaigham ,&nbsp;R.J. Bertelsen ,&nbsp;S.C. Dharmage ,&nbsp;V. Schlünssen ,&nbsp;N.O. Jögi ,&nbsp;L. Palacios Gomez ,&nbsp;M. Holm ,&nbsp;A. Oudin ,&nbsp;M.J. Abramson ,&nbsp;T. Sigsgaard ,&nbsp;R. Jõgi ,&nbsp;C. Svanes ,&nbsp;A.C. Olin ,&nbsp;B. Forsberg ,&nbsp;C. Janson ,&nbsp;E. Nerpin ,&nbsp;A. Johannessen ,&nbsp;A. Malinovschi","doi":"10.1016/j.niox.2024.06.001","DOIUrl":"10.1016/j.niox.2024.06.001","url":null,"abstract":"<div><h3>Background</h3><p>Parental allergic diseases and smoking influence respiratory disease in the offspring but it is not known whether they influence fractional exhaled nitric oxide (FeNO) in the offspring. We investigated whether parental allergic diseases, parental smoking and FeNO levels in parents were associated with FeNO levels in their offspring.</p></div><div><h3>Methods</h3><p>We studied 609 offspring aged 16–47 years from the Respiratory Health in Northern Europe, Spain and Australia generation (RHINESSA) study with parental information from the Respiratory Health in Northern Europe (RHINE) III study and the European Community Respiratory Health Survey (ECRHS) III. Linear regression models were used to assess the association between offspring FeNO and parental FeNO, allergic rhinitis, asthma and smoking, while adjusting for potential confounding factors.</p></div><div><h3>Results</h3><p>Parental allergic rhinitis was significantly associated with higher FeNO in the offspring, both on the paternal and maternal side (percent change: 20.3 % [95%CI 5.0–37.7], p = 0.008, and 13.8 % [0.4–28.9], p = 0.043, respectively). Parental allergic rhinitis with asthma in any parent was also significantly associated with higher offspring FeNO (16.2 % [0.9–33.9], p = 0.037). However, parental asthma alone and smoking were not associated with offspring FeNO. Parental FeNO was not associated with offspring FeNO after full adjustments for offspring and parental factors.</p></div><div><h3>Conclusions</h3><p>Parental allergic rhinitis but not parental asthma was associated with higher levels of FeNO in offspring. These findings suggest that parental allergic rhinitis status should be considered when interpreting FeNO levels in offspring beyond childhood.</p></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"149 ","pages":"Pages 60-66"},"PeriodicalIF":3.9,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1089860324000764/pdfft?md5=82733d116ee630e9b41a516c46b1baac&pid=1-s2.0-S1089860324000764-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141321323","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}

{"title":"Endoplasmic reticulum protein of 57 kDa sulfhydration promotes intestinal calcium absorption to attenuate primary osteoporosis","authors":"Huifang Liu ,&nbsp;Yang Zheng ,&nbsp;Fuming Li ,&nbsp;Bin Geng ,&nbsp;Feng Liao","doi":"10.1016/j.niox.2024.05.004","DOIUrl":"10.1016/j.niox.2024.05.004","url":null,"abstract":"<div><p>Endogenous hydrogen sulfide (H₂S) plays an important role in bone metabolism. However, the exact role of H₂S in intestinal calcium and phosphorus absorption and its potential in preventing and treating primary osteoporosis remains unknown. Therefore, this study aimed to investigate the potential of H₂S in promoting intestinal calcium and phosphorus absorption and alleviating primary osteoporosis. We measured the apparent absorptivity of calcium, femoral bone density, expression and sulfhydration of the duodenal endoplasmic reticulum protein of 57 kDa (ERp57), duodenal cystathionine γ-lyase (CSE) expression, and serum H₂S content in adult and old CSE-knockout and wild-type mice. We also assessed intracellular reactive oxygen species (ROS) and Ca²⁺ content in CSE-overexpressing or knockout intestinal epithelial cell (IEC)-6 cells. In senile mice, CSE knockout decreased endogenous H₂S, ERp57 sulfhydration, and intestinal calcium absorption and worsened osteoporosis, which were partially reversed by GYY4137, an H₂S donor. CSE overexpression in IEC-6 cells increased ERp57 sulfhydration, protein kinase A and C activity, and intracellular Ca²⁺, whereas CSE knockout exerted the opposite effects. Furthermore, hydrogen peroxide (H₂O₂) stimulation had similar effects as in CSE knockout, which were reversed by pretreatment with sodium hydrosulfide before H₂O₂ stimulation and restored by DL-dithiothreitol. These findings suggest that H₂S attenuates primary osteoporosis by preventing ROS-induced ERp57 damage in intestinal epithelial cells by enhancing ERp57 activity and promoting intestinal calcium absorption, thereby aiding in developing therapeutic interventions to prevent osteoporosis.</p></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"149 ","pages":"Pages 32-40"},"PeriodicalIF":3.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1089860324000752/pdfft?md5=459653b0d397adc1664e7eb514afff00&pid=1-s2.0-S1089860324000752-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141238317","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}

{"title":"Leveraging the redundancy of S-denitrosylases in response to S-nitrosylation of caspases: Experimental strategies and beyond","authors":"Surupa Chakraborty,&nbsp;Akansha Mishra ,&nbsp;Ankita Choudhuri ,&nbsp;Tamal Bhaumik,&nbsp;Rajib Sengupta","doi":"10.1016/j.niox.2024.05.002","DOIUrl":"10.1016/j.niox.2024.05.002","url":null,"abstract":"<div><p>Redox-based protein posttranslational modifications, such as S-nitrosylation of critical, active site cysteine thiols have garnered significant clinical attention and research interest, reasoning for one of the crucial biological implications of reactive messenger molecule, nitric oxide in the cellular repertoire. The stringency of the S-(de)nitrosylation-based redox switch governs the activity and contribution of several susceptible enzymes in signal transduction processes and diverse pathophysiological settings, thus establishing it as a transient yet reasonable, and regulated mechanism of NO adduction and release. Notably, endogenous proteases like cytosolic and mitochondrial caspases with a molecular weight ranging from 33 to 55 kDa are susceptible to performing this biochemistry in the presence of major oxidoreductases, which further unveils the enormous redox-mediated regulational control of caspases in the etiology of diseases. In addition to advancing the progress of the current state of understanding of ‘redox biochemistry’ in the field of medicine and enriching the existing dynamic S-nitrosoproteome, this review stands as a testament to an unprecedented shift in the underpinnings for redundancy and redox relay between the major redoxin/antioxidant systems, fine-tuning of which can command the apoptotic control of caspases at the face of nitro-oxidative stress. These intricate functional overlaps and cellular backups, supported rationally by kinetically favorable reaction mechanisms suggest the physiological relevance of identifying and involving such cognate substrates for cellular S-denitrosylases that can shed light on the bigger picture of extensively proposing targeted therapies and redox-based drug designing to potentially alleviate the side effects of NOx/ROS in disease pathogenesis.</p></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"149 ","pages":"Pages 18-31"},"PeriodicalIF":3.9,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial dysfunction in Sickle Cell Disease: Strategies for the treatment","authors":"Aline Renata Pavan ,&nbsp;Barbara Terroni ,&nbsp;Jean Leandro Dos Santos","doi":"10.1016/j.niox.2024.05.003","DOIUrl":"10.1016/j.niox.2024.05.003","url":null,"abstract":"<div><p>Sickle Cell Anemia (SCA), is an inherited hemoglobinopathy characterized by the presence of an abnormal hemoglobin (HbS), being the most prevalent sickle cell disease (SCD). SCA is characterized by vascular endothelial dysfunction, which contributes significantly to various clinical conditions, including but not limited to pulmonary hypertension, priapism, cutaneous leg ulceration, and stroke. The pathophysiology of endothelial dysfunction (ED) in SCA is a multifaceted process involving a chronic inflammatory and hypercoagulable state. Key factors include hemolysis-associated elements like reduced arginine and nitric oxide (NO) availability, elevated levels of vascular adhesion molecules, the uncoupling effect of NO synthase, heightened arginase activity, an environment characterized by oxidative stress with the production of reactive oxygen and nitrogen species, and occurrences of ischemia-reperfusion injury, along with apolipoprotein A-1 depletion. The urgency for novel interventions addressing ED is evident. Presently, there is a focus on investigating small molecules that disrupt the arginine-nitric oxide pathway, exhibiting anti-inflammatory and antioxidant properties while diminishing levels of cellular and vascular adhesion molecules. In this mini-review article, we delve into the progress made in strategies for treating ED in SCD with the aim of cultivating insights for drug design.</p></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"149 ","pages":"Pages 7-17"},"PeriodicalIF":3.9,"publicationDate":"2024-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141162022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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 protects intestinal mucosal barrier function and prevents acute graft rejection after intestinal transplantation: A mini-review","authors":"George J. Dugbartey ,&nbsp;Deborah Nanteer ,&nbsp;Ivy Osae","doi":"10.1016/j.niox.2024.05.001","DOIUrl":"10.1016/j.niox.2024.05.001","url":null,"abstract":"<div><p>Intestinal transplantation is a complex technical procedure that provides patients suffering from end-stage intestinal failure an opportunity to enjoy improved quality of life, nutrition and survival. Compared to other types of organ transplants, it is a relatively new advancement in the field of organ transplantation. Nevertheless, great advances have been made over the past few decades to the present era, including the use of ischemic preconditioning, gene therapy, and addition of pharmacological supplements to preservation solutions. However, despite these strides, intestinal transplantation is still a challenging endeavor due to several factors. Notable among them is ischemia-reperfusion injury (IRI), which results in loss of cellular integrity and mucosal barrier function. In addition, IRI causes graft failure, delayed graft function, and decreased graft and recipient survival. This has necessitated the search for novel therapeutic avenues and improved transplantation protocols to prevent or attenuate intestinal IRI. Among the many candidate agents that are being investigated to combat IRI and its associated complications, nitric oxide (NO). NO is an endogenously produced gaseous signaling molecule with several therapeutic properties. The purpose of this mini-review is to discuss IRI and its related complications in intestinal transplantation, and NO as an emerging pharmacological tool against this challenging pathological condition. i</p></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"149 ","pages":"Pages 1-6"},"PeriodicalIF":3.9,"publicationDate":"2024-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141162025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}