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Article ; Online: Correction: Angiotensin-(1-9) prevents Angiotensin II-induced endothelial apoptosis through CNPY2/PERK pathway.

Guo, Chun-Ling / Liu, Hui-Min / Li, Bao / Lu, Zhao-Yang

Apoptosis : an international journal on programmed cell death

2023 Volume 28, Issue 9-10, Page(s) 1496–1499

Language	English
Publishing date	2023-07-20
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	1452360-7
ISSN	1573-675X ; 1360-8185
ISSN (online)	1573-675X
ISSN	1360-8185
DOI	10.1007/s10495-023-01876-8
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Article ; Online: Angiotensin-(1-9) prevents angiotensin II-induced endothelial apoptosis through CNPY2/PERK pathway.

Guo, Chun-Ling / Liu, Hui-Min / Li, Bao / Lu, Zhao-Yang

Apoptosis : an international journal on programmed cell death

2022 Volume 28, Issue 3-4, Page(s) 379–396

Abstract: Endothelial apoptosis caused by activation of renin-angiotensin system (RAS) plays a vital part in the occurrence and progress of hypertension. Angiotensin-(1-9) (Ang-(1-9)) is a peptide of the counter-regulatory non-classical RAS with anti-hypertensive ... ...

Abstract	Endothelial apoptosis caused by activation of renin-angiotensin system (RAS) plays a vital part in the occurrence and progress of hypertension. Angiotensin-(1-9) (Ang-(1-9)) is a peptide of the counter-regulatory non-classical RAS with anti-hypertensive effects in vascular endothelial cells (ECs). However, the mechanism of action remains unclear. Considering that the endothelial apoptosis was closely related to endoplasmic reticulum stress (ERS) and mitochondrial function. Herein, we aimed to elucidate the effects of Ang-(1-9) on endothelial apoptosis and the underlying molecular mechanism in angiotensin II (Ang II) induced hypertension. In human umbilical vascular endothelial cells (HUVECs), we observed Ang-(1-9) inhibited Ang II-induced ERS associated endothelial apoptosis. Mechanically, Ang-(1-9) inhibited endothelial apoptosis by blocking CNPY2/PERK mediated CaMKII/Drp1-dependent mitochondrial fission and eIF2α/CHOP signal. Consistent with above effects in HUVECs, in Ang II-induced hypertensive mice, we found administration of exogenous Ang-(1-9) attenuated endothelial apoptosis and arterial blood pressure, which were mediated by CNPY2/PERK signaling pathway. Our study indicated Ang-(1-9) inhibited Ang II-induced hypertension through CNPY2/PERK pathway. These findings may provide new insights for prevention and treatment of hypertension in future.
MeSH term(s)	Humans ; Animals ; Mice ; Angiotensin II/pharmacology ; Angiotensin II/metabolism ; Human Umbilical Vein Endothelial Cells ; Apoptosis ; Signal Transduction ; Hypertension/metabolism ; Adaptor Proteins, Signal Transducing/metabolism
Chemical Substances	Angiotensin II (11128-99-7) ; CNPY2 protein, human ; Adaptor Proteins, Signal Transducing
Language	English
Publishing date	2022-11-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1452360-7
ISSN	1573-675X ; 1360-8185
ISSN (online)	1573-675X
ISSN	1360-8185
DOI	10.1007/s10495-022-01793-2
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Article ; Online: Dapagliflozin Suppresses Isoprenaline-Induced Cardiac Hypertrophy Through Inhibition of Mitochondrial Fission.

Yang, Zhuo-Jing / Guo, Chun-Ling / Gong, Yu-Xin / Li, Long / Wang, Li-Li / Liu, Hui-Min / Cao, Ji-Min / Lu, Zhao-Yang

Journal of cardiovascular pharmacology

2024 Volume 83, Issue 2, Page(s) 193–204

Abstract: Abstract: Dapagliflozin (DAPA) is a novel oral hypoglycemic agent, and there is increasing evidence that DAPA has a protective effect against cardiovascular disease. The study aimed to investigate how DAPA inhibits cardiac hypertrophy and explore its ... ...

Abstract	Abstract: Dapagliflozin (DAPA) is a novel oral hypoglycemic agent, and there is increasing evidence that DAPA has a protective effect against cardiovascular disease. The study aimed to investigate how DAPA inhibits cardiac hypertrophy and explore its potential mechanisms. By continuously infusing isoprenaline (ISO) for 2 weeks using a subcutaneous osmotic pump, a cardiac hypertrophic model was established in male C57BL/6 mice. On day 14 after surgery, echocardiography showed that left ventricle mass (LV mass), interventricular septum, left ventricle posterior wall diastole, and left ventricular posterior wall systole were significantly increased, and ejection fraction was decreased compared with control mice. Masson and Wheat Germ Agglutinin staining indicated enhanced myocardial fibrosis and cell morphology compared with control mice. Importantly, these effects were inhibited by DAPA treatment in ISO-induced mice. In H9c2 cells and neonatal rat cardiomyocytes, we found that mitochondrial fragmentation and mitochondrial oxidative stress were significantly augmented in the ISO-induced group. However, DAPA rescued the cardiac hypertrophy in ISO-induced H9c2 cells and neonatal rat cardiomyocytes. Mechanistically, we found that DAPA restored the PIM1 activity in ISO-induced H9c2 cells and subsequent increase in dynamin-associated protein 1 (Drp1) phosphorylation at S616 and decrease in Drp1 phosphorylation at S637 in ISO-induced cells. We found that DAPA mitigated ISO-induced cardiac hypertrophy by suppressing Drp1-mediated mitochondrial fission in a PIM1-dependent fashion.
MeSH term(s)	Rats ; Mice ; Male ; Animals ; Isoproterenol/pharmacology ; Mitochondrial Dynamics ; Mice, Inbred C57BL ; Cardiomegaly/metabolism ; Myocytes, Cardiac ; Benzhydryl Compounds ; Glucosides
Chemical Substances	Isoproterenol (L628TT009W) ; dapagliflozin (1ULL0QJ8UC) ; Benzhydryl Compounds ; Glucosides
Language	English
Publishing date	2024-02-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	391970-5
ISSN	1533-4023 ; 0160-2446
ISSN (online)	1533-4023
ISSN	0160-2446
DOI	10.1097/FJC.0000000000001518
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Article: Selenium Attenuates Doxorubicin-Induced Cardiotoxicity Through Nrf2-NLRP3 Pathway

Yang, Hai-Bing / Lu, Zhao-Yang / Yuan, Wei / Li, Wei-Dong / Mao, Shang

Biological trace element research. 2022 June, v. 200, no. 6

2022

Abstract: Selenium (Se), an essential nutrient for humans, has been reported to possess cardioprotective effect. However, the protective effects of Se against doxorubicin (DOX)-induced cardiotoxicity and the underlying mechanism are rarely reported. In this study, ...

Abstract	Selenium (Se), an essential nutrient for humans, has been reported to possess cardioprotective effect. However, the protective effects of Se against doxorubicin (DOX)-induced cardiotoxicity and the underlying mechanism are rarely reported. In this study, we sought to explore whether Se protected against DOX-induced cardiotoxicity by inhibiting Nrf2-NLRP3 pathway. We found that Se treatment effectively alleviated DOX-induced myocardial dysfunctions, decreasing plasma markers associated with myocardial injury. Moreover, Se treatment significantly inhibited DOX-induced oxidative damages and pro-inflammatory cytokine expression in heart tissues. Furthermore, Se treatment markedly promoted the expression of Nrf2 and prevented the activation of NLRP3 inflammasome. Importantly, suppression of Nrf2 abolished the cardioprotective effects of Se and diminished the inhibition of Se on NLRP3 inflammasome. Collectively, our study demonstrated that Se might protect against DOX-induced cardiotoxicity via regulating Nrf2-NLRP3 pathway. Se supplementation may be a potential therapeutic strategy to protect against DOX-induced cardiac injury.
Keywords	cardioprotective effect ; cardiotoxicity ; cytokines ; doxorubicin ; heart ; inflammasomes ; research ; therapeutics ; trace elements
Language	English
Dates of publication	2022-06
Size	p. 2848-2856.
Publishing place	Springer US
Document type	Article
ZDB-ID	445336-0
ISSN	1559-0720 ; 0163-4984
ISSN (online)	1559-0720
ISSN	0163-4984
DOI	10.1007/s12011-021-02891-z
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Dynamic Immune/Inflammation Precision Medicine: The Good and the Bad Inflammation in Infection and Cancer.

Rossi, Jean-François / Lu, Zhao Yang / Massart, Cesare / Levon, Kalle

Frontiers in immunology

2021 Volume 12, Page(s) 595722

Abstract: Normal or "good" inflammation process starts from a local cellular response against injury or any infectious agent, with the activation of neutrophils, macrophages, Langerhans cells, dendritic cells, and innate immune cells. Cytokines and chemokines are ... ...

Abstract	Normal or "good" inflammation process starts from a local cellular response against injury or any infectious agent, with the activation of neutrophils, macrophages, Langerhans cells, dendritic cells, and innate immune cells. Cytokines and chemokines are produced to amplify the local inflammatory process followed by the migration of immune cells to the regional lymph nodes where adaptive immune response is initiated. Systemic inflammation enhances the biological response to mobilize additional cells from central and peripheral immune/hematopoietic system. Local mechanisms to limit inflammation are initiated and lead to healing. During the normal inflammatory process, there is a balance between the production of inflammatory chemokines/cytokines such as Tumor Necrosis Factor (TNF)-α, interleukin (IL)-6 and IL-1 and the production of compounds that limit inflammation and have an immune suppressive effect, such as IL-10 and Transforming Factor (TGF) β. IL-6 and IL-6/soluble IL-6 Receptor (R) complex stimulate liver cells to produce inflammatory proteins, which represents the systemic inflammation response. The magnitude and the duration of the systemic inflammatory response are linked to the cause, under genetic and epigenetic control. Significant inflammation as seen in septic shock, in severe forms of infections or in certain active cancers, represents the "bad inflammation", correlated with a poor prognosis. In addition, the persistence of a chronic smoldering inflammation may lead to pathological situations which are observed in the majority of inflammatory, degenerative, dysmetabolic, or dysimmune diseases and cancer. Chronic smoldering inflammation is a cross between different pathological situations possibly linked. In addition, within the tumor microenvironment, inflammatory process results from different cellular mechanisms modulated by metabolic and vascular changes. On the contrary, a limited and balanced inflammation initiates the normal immune response, including the adaptive response which amplifies any immunotherapy, including vaccines. Immune checkpoint inhibitors and chimeric antigen receptor (CAR) T-cells are associated with cytokine release syndrome, a clinical risk leading to the use of anti-cytokine drugs. Nowadays, it is time to monitor the dynamic inflammatory process for a better immune precision medicine in both infections and cancer.
MeSH term(s)	Animals ; Biomarkers ; Disease Management ; Disease Susceptibility/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Inflammation/diagnosis ; Inflammation/etiology ; Inflammation/therapy ; Inflammation Mediators ; Neoplasms/diagnosis ; Neoplasms/etiology ; Neoplasms/therapy ; Precision Medicine
Chemical Substances	Biomarkers ; Inflammation Mediators
Language	English
Publishing date	2021-02-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.595722
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Mesh erosion into the colon following repair of parastomal hernia: A case report.

Zhang, Yu / Lin, Han / Liu, Jia-Ming / Wang, Xin / Cui, Yi-Feng / Lu, Zhao-Yang

World journal of gastrointestinal surgery

2022 Volume 15, Issue 2, Page(s) 294–302

Abstract: Background: In recent years, mesh has become a standard repair method for parastomal hernia surgery due to its low recurrence rate and low postoperative pain. However, using mesh to repair parastomal hernias also carries potential dangers. One of these ... ...

Abstract	Background: In recent years, mesh has become a standard repair method for parastomal hernia surgery due to its low recurrence rate and low postoperative pain. However, using mesh to repair parastomal hernias also carries potential dangers. One of these dangers is mesh erosion, a rare but serious complication following hernia surgery, particularly parastomal hernia surgery, and has attracted the attention of surgeons in recent years. Case summary: Herein, we report the case of a 67-year-old woman with mesh erosion after parastomal hernia surgery. The patient, who underwent parastomal hernia repair surgery 3 years prior, presented to the surgery clinic with a complaint of chronic abdominal pain upon resuming defecation through the anus. Three months later, a portion of the mesh was excreted from the patient's anus and was removed by a doctor. Imaging revealed that the patient's colon had formed a t-branch tube structure, which was formed by the mesh erosion. The surgery reconstructed the structure of the colon and eliminated potential bowel perforation. Conclusion: Surgeons should consider mesh erosion since it has an insidious development and is difficult to diagnose at the early stage.
Language	English
Publishing date	2022-04-21
Publishing country	United States
Document type	Case Reports
ZDB-ID	2573700-4
ISSN	1948-9366
ISSN	1948-9366
DOI	10.4240/wjgs.v15.i2.294
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Article ; Online: Immune precision medicine for cancer: a novel insight based on the efficiency of immune effector cells.

Rossi, Jean-François / Céballos, Patrice / Lu, Zhao-Yang

Cancer communications (London, England)

2019 Volume 39, Issue 1, Page(s) 34

Abstract: Cancer cell growth is associated with immune surveillance failure. Nowadays, restoring the desired immune response against cancer cells remains a major therapeutic strategy. Due to the recent advances in biological knowledge, efficient therapeutic tools ... ...

Abstract	Cancer cell growth is associated with immune surveillance failure. Nowadays, restoring the desired immune response against cancer cells remains a major therapeutic strategy. Due to the recent advances in biological knowledge, efficient therapeutic tools have been developed to support the best bio-clinical approaches for immune precision therapy. One of the most important successes in immune therapy is represented by the applicational use of monoclonal antibodies, particularly the use of rituximab for B-cell lymphoproliferative disorders. More recently, other monoclonal antibodies have been developed, to inhibit immune checkpoints within the tumor microenvironment that limit immune suppression, or to enhance some immune functions with immune adjuvants through different targets such as Toll-receptor agonists. The aim is to inhibit cancer proliferation by the diminishing/elimination of cancer residual cells and clinically improving the response duration with no or few adverse effects. This effect is supported by enhancing the number, functions, and activity of the immune effector cells, including the natural killer (NK) lymphocytes, NKT-lymphocytes, γδ T-lymphocytes, cytotoxic T-lymphocytes, directly or indirectly through vaccines particularly with neoantigens, and by lowering the functions of the immune suppressive cells. Beyond these new therapeutics and their personalized usage, new considerations have to be taken into account, such as epigenetic regulation particularly from microbiota, evaluation of transversal functions, particularly cellular metabolism, and consideration to the clinical consequences at the body level. The aim of this review is to discuss some practical aspects of immune therapy, giving to clinicians the concept of immune effector cells balancing between control and tolerance. Immunological precision medicine is a combination of modern biological knowledge and clinical therapeutic decisions in a global vision of the patient.
MeSH term(s)	Cancer Vaccines ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Disease Susceptibility/immunology ; Humans ; Immunotherapy/methods ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Neoplasms/diagnosis ; Neoplasms/immunology ; Neoplasms/therapy ; Precision Medicine/methods ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Treatment Outcome
Chemical Substances	Cancer Vaccines
Language	English
Publishing date	2019-06-14
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2523-3548
ISSN (online)	2523-3548
DOI	10.1186/s40880-019-0379-3
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Article ; Online: Selenium Attenuates Doxorubicin-Induced Cardiotoxicity Through Nrf2-NLRP3 Pathway.

Yang, Hai-Bing / Lu, Zhao-Yang / Yuan, Wei / Li, Wei-Dong / Mao, Shang

Biological trace element research

2021 Volume 200, Issue 6, Page(s) 2848–2856

Abstract	Selenium (Se), an essential nutrient for humans, has been reported to possess cardioprotective effect. However, the protective effects of Se against doxorubicin (DOX)-induced cardiotoxicity and the underlying mechanism are rarely reported. In this study, we sought to explore whether Se protected against DOX-induced cardiotoxicity by inhibiting Nrf2-NLRP3 pathway. We found that Se treatment effectively alleviated DOX-induced myocardial dysfunctions, decreasing plasma markers associated with myocardial injury. Moreover, Se treatment significantly inhibited DOX-induced oxidative damages and pro-inflammatory cytokine expression in heart tissues. Furthermore, Se treatment markedly promoted the expression of Nrf2 and prevented the activation of NLRP3 inflammasome. Importantly, suppression of Nrf2 abolished the cardioprotective effects of Se and diminished the inhibition of Se on NLRP3 inflammasome. Collectively, our study demonstrated that Se might protect against DOX-induced cardiotoxicity via regulating Nrf2-NLRP3 pathway. Se supplementation may be a potential therapeutic strategy to protect against DOX-induced cardiac injury.
MeSH term(s)	Apoptosis ; Cardiotoxicity/drug therapy ; Cardiotoxicity/metabolism ; Cardiotoxicity/prevention & control ; Doxorubicin/toxicity ; Humans ; Inflammasomes ; Myocytes, Cardiac/metabolism ; NF-E2-Related Factor 2/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein ; Oxidative Stress ; Selenium/metabolism
Chemical Substances	Inflammasomes ; NF-E2-Related Factor 2 ; NLR Family, Pyrin Domain-Containing 3 Protein ; Doxorubicin (80168379AG) ; Selenium (H6241UJ22B)
Language	English
Publishing date	2021-08-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	445336-0
ISSN	1559-0720 ; 0163-4984
ISSN (online)	1559-0720
ISSN	0163-4984
DOI	10.1007/s12011-021-02891-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Optimisation of anti-interleukin-6 therapy: Precision medicine through mathematical modelling.

Rossi, Jean-François / Chiang, Hao-Chun / Lu, Zhao-Yang / Levon, Kalle / van Rhee, Frits / Kanhai, Karan / Fajgenbaum, David C / Klein, Bernard

Frontiers in immunology

2022 Volume 13, Page(s) 919489

Abstract: Background: Dysregulated interleukin (IL)-6 production can be characterised by the levels present, the kinetics of its rise and its inappropriate location. Rapid, excessive IL-6 production can exacerbate tissue damage in vital organs. In this situation, ...

Abstract	Background: Dysregulated interleukin (IL)-6 production can be characterised by the levels present, the kinetics of its rise and its inappropriate location. Rapid, excessive IL-6 production can exacerbate tissue damage in vital organs. In this situation, therapy with an anti-IL-6 or anti-IL-6 receptor (IL-6R) monoclonal antibody, if inappropriately dosed, may be insufficient to fully block IL-6 signalling and normalise the immune response. Methods: We analysed inhibition of C-reactive protein (CRP) - a biomarker for IL-6 activity - in patients with COVID-19 or idiopathic multicentric Castleman disease (iMCD) treated with tocilizumab (anti-IL-6R) or siltuximab (anti-IL-6), respectively. We used mathematical modelling to analyse how to optimise anti-IL-6 or anti-IL-6R blockade for the high levels of IL-6 observed in these diseases. Results: IL-6 signalling was insufficiently inhibited in patients with COVID-19 or iMCD treated with standard doses of anti-IL-6 therapy. Patients whose disease worsened throughout therapy had only partial inhibition of CRP production. Our model demonstrated that, in a scenario representative of iMCD with persistent high IL-6 production not controlled by a single dose of anti-IL-6 therapy, repeated administration more effectively inhibited IL-6 activity. In a situation with rapid, high, dysregulated IL-6 production, such as severe COVID-19 or a cytokine storm, repeated daily administration of an anti-IL-6/anti-IL-6R agent, or alternating daily doses of anti-IL-6 and anti-IL-6R therapies, could neutralise IL-6 activity. Conclusion: In clinical practice, IL-6 inhibition should be individualised based on pathophysiology to achieve full blockade of CRP production. Funding: EUSA Pharma funded medical writing assistance and provided access to the phase II clinical data of siltuximab for analysis.
MeSH term(s)	C-Reactive Protein/therapeutic use ; Castleman Disease/drug therapy ; Cytokine Release Syndrome ; Humans ; Precision Medicine ; COVID-19 Drug Treatment
Chemical Substances	C-Reactive Protein (9007-41-4)
Language	English
Publishing date	2022-07-19
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.919489
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Article ; Online: Effect of Diallyl Trisulfide on Ischemic Tissue Injury and Revascularization in a Diabetic Mouse Model.

Yang, Hai-Bing / Liu, Hui-Min / Yan, Jin-Chuan / Lu, Zhao-Yang

Journal of cardiovascular pharmacology

2018 Volume 71, Issue 6, Page(s) 367–374

Abstract: Background and objective: Allitridin [diallyl trisulfide (DATS)] is an extract from garlic (Allium sativum) that putatively improves endothelial function and is protective against cardiovascular diseases. Endothelial dysfunction after tissue ischemia in ...

Abstract	Background and objective: Allitridin [diallyl trisulfide (DATS)] is an extract from garlic (Allium sativum) that putatively improves endothelial function and is protective against cardiovascular diseases. Endothelial dysfunction after tissue ischemia in diabetic patients is partially due to poor angiogenic response. This study investigated whether DATS may improve angiogenesis in a diabetic mouse model with hind limb ischemia. Methods: Streptozotocin was administered by intraperitoneal injection to establish the model of diabetes in male C57BL/6 mice. After 14 days, nondiabetic and diabetic mice (n = 24, each) underwent unilateral hind limb ischemia by femoral artery ligation. The mice were apportioned to 4 groups: nondiabetic treated (or not) with DATS and diabetic treated (or not) with DATS. DATS treatment consisted of a single daily intraperitoneal injection of 500 μg·kg·d for 14 days, beginning on the day of induced ischemia. Ischemia was scored by standard criteria. Blood perfusion was determined using thermal infrared imaging. Tissue capillary density and oxidative stress levels were measured by immunohistochemistry and immunofluorescence, respectively. Serum lipids were measured by enzymatic colorimetric assay. Fasting serum insulin was detected using an insulin enzyme-linked immunosorbent assay kit. Nitric oxide (NO) metabolites and protein carbonyls in tissues were determined by enzyme-linked immunosorbent assay. Targeted protein concentrations were measured by western blotting. Results: At 14 days after ligation, the ischemic skeletal muscle of the streptozotocin-induced diabetic mice had lower levels of endothelial NO synthase, phosphorylated endothelial NO synthase, and vascular endothelial growth factor compared with nondiabetic group. In addition, the hind limb blood perfusion, capillary density, and NO bioactivity were lower in the diabetic group, whereas oxidative stress and protein carbonyl levels were higher. These changes were ameliorated by DATS treatment. Conclusions: DATS treatment of diabetic mice promoted revascularization in ischemic tissue.
MeSH term(s)	Allyl Compounds/pharmacology ; Angiogenesis Inducing Agents/pharmacology ; Animals ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/physiopathology ; Diabetic Angiopathies/drug therapy ; Diabetic Angiopathies/etiology ; Diabetic Angiopathies/metabolism ; Diabetic Angiopathies/physiopathology ; Hindlimb ; Ischemia/drug therapy ; Ischemia/etiology ; Ischemia/metabolism ; Ischemia/physiopathology ; Male ; Mice, Inbred C57BL ; Muscle, Skeletal/blood supply ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Neovascularization, Physiologic/drug effects ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Oxidative Stress/drug effects ; Phosphorylation ; Protein Carbonylation/drug effects ; Regional Blood Flow ; Sulfides/pharmacology ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Allyl Compounds ; Angiogenesis Inducing Agents ; Sulfides ; Vascular Endothelial Growth Factor A ; vascular endothelial growth factor A, mouse ; diallyl trisulfide (0ZO1U5A3XX) ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, mouse (EC 1.14.13.39)
Language	English
Publishing date	2018-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	391970-5
ISSN	1533-4023 ; 0160-2446
ISSN (online)	1533-4023
ISSN	0160-2446
DOI	10.1097/FJC.0000000000000579
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