Chronic cigarette smoke exposure triggers a vicious cycle of leukocyte and endothelial-mediated oxidant stress that results in vascular dysfunction

El‐Mahdy, Mohamed A.; Abdelghany, Tamer M.; Hemann, Craig; Ewees, Mohamed G; Mahgoup, Elsayed M.; Eid, Mahmoud S; Shalaan, Mahmoud T; Alzarie, Yasmin A.; Zweíer, Jay L.

doi:10.1152/ajpheart.00657.2019

Cited by 35 publications

(20 citation statements)

References 88 publications

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“…The supernatant (0.5 mL) was mixed with 2 mL of 0.3 M disodium hydrogen phosphate buffer (pH 8.4) and 0.4 mL of distilled water. Then, 0.25 mL of 0.001 M freshly prepared DTNB 5 50–dithiobis (2-nitrobenzoic acid) dissolved in 1% w/v sodium citrate] was added to the reaction mixture, and incubated for 10 min. The absorbance of the yellow colored complex was noted spectrophotometrically at 412 nm.…”

Section: Methodsmentioning

confidence: 99%

“…[ 2 3 ] Vascular endothelial dysfunction (VED) of microvessels results in reduced activation of endothelial nitric oxide synthase (eNOS), reduced generation and bioavailability of nitric oxide (NO) and increased production of reactive oxygen species (ROS). [ 4 5 ] VED, which is one of the important among the earliest stages has been associated in the pathogenesis of hypertension, coronary artery diseases and nephropathy. [ 6 7 ] A correlation between VED and kidney injury has been demonstrated in various studies.…”

Section: Introductionmentioning

confidence: 99%

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Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase

Chakkarwar¹,

Kawtikwar²

2021

Indian J Nephrol

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Objective: The present study investigated the possible effect of fenofibrate (peroxisome proliferator-activated receptors-α agonist) in nicotine-induced acute kidney injury (AKI) in rats. Materials and Methods: Nicotine (2 mg/kg/day, intraperitoneally) was administered for 4 weeks to induce AKI in rats. Lipid profile and renal oxidative stress were measured and expression of mRNA for eNOS was assessed using reverse transcription-polymerase chain reaction along with serum and renal tissue nitrite levels. Serum creatinine, blood urea nitrogen and microproteinuria were estimated along with the kidney histology, as markers of kidney function. Treatment with fenofibrate (30 mg/kg per oral, 4 weeks) was initiated 3 days before the administration of nicotine and continued for 4 weeks from the day of administration of nicotine. Results: Nicotine administered rats developed apparent AKI confirmed by elevated markers of kidney function and noticeable glomerulosclerosis and tubular cell degeneration. Nicotine decreases the expression of mRNA for eNOS, along with serum and renal tissue nitrite levels. In addition, nicotine showed significantly lipid alteration beside decrease oxidative stress, assessed in terms of increase in serum thiobarbituric acid reactive substance and a marked decrease in tissue reduced glutathione. However, fenofibrate significantly prevented the development of nicotine-AKI by reducing serum creatinine, BUN, and urinary protein, normalizing the lipid profile, reducing renal oxidative stress, increases the eNOS expression and concentration of serum and renal nitrate levels. Conclusion: Fenofibrate attenuates nicotine-induced AKI, via its antihyperlipidemic and antioxidant property. Moreover, fenofibrate induced upregulation of eNOS expression additionally play key roles in the improvement of nicotine-induced AKI could be the future alternative.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase

Chakkarwar¹,

Kawtikwar²

2021

Indian J Nephrol

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“…Previous studies have shown that exposure to tobacco smoke impairs the function of vascular endothelial cells, but most of the research focused on coronary arteries. [32][33][34] Further research is needed on the pathogenesis of RAP caused by smoking and whether smoking cessation can reduce the risk of recurrence. Anyway, physicians should be advising patients to quit smoking at all times.…”

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confidence: 99%

Risk Factors for Recurrent Pancreatitis After First Episode of Acute Pancreatitis

Sun¹,

Jin²,

Zhu³

et al. 2022

IJGM

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In recent years, the cure rate of acute pancreatitis (AP) has increased gradually, but the morbidity of recurrent acute pancreatitis (RAP) has not decreased. Patients with RAP have a poor quality of life and are more likely to develop into chronic pancreatitis. To investigate the risk factors of RAP after first pancreatitis attack is very necessary. Methods: Patients with first episode AP admitted to Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine from January 2018 to May 2021 were included in this retrospective study, and follow-up was 3-45 months after discharge. The patients information were collected from medical records including laboratory tests and auxiliary inspection of their hospitalization. Univariate and multivariate Cox regression analysis were used to explore the risk factors of RAP. Cumulative risk of RAP was plotted using Kaplan-Meier curves. Results: A total of 592 patients were enrolled in the study and 81 (13.7%) of the patients developed RAP. Among those RAP patients, the majority (67.9%) were men, with a median age of 43 years. The most common etiology of RAP was hypertriglyceridemia (38.3%). Multivariate Cox analysis showed that smoking history (p < 0.001), infected pancreatic necrosis occurred during first admission (p = 0.005), and high low-density lipoprotein cholesterol (LDLc) level (p < 0.001) were significant independent risk factors for RAP. Patients with the above independent risk factors had increased 3-year cumulative risk of recurrence (32.2%, 45.5%, 28.9%, respectively). Conclusion: Smoking history, infected pancreatic necrosis, and high LDLc level were the most decisive risk factors for RAP. Attention should be paid to the patients with the above factors.

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“…It has been suggested that smoke exposure primes leukocytes to promote aortic degradation. Cigarette smoke also activates endothelial cells to express adhesion molecules and chemokines promoting leukocyte infiltration into the aortic wall [ 20 ]. In one mouse study, adoptive transfer of leukocytes from mice exposed to cigarette smoke promoted induction of larger aneurysms in an elastase model [ 21 ].…”

Section: Clinical Risk Factors For Aaa Rupturementioning

confidence: 99%

Risk Factors and Mouse Models of Abdominal Aortic Aneurysm Rupture

Krishna

Morton

et al. 2020

IJMS

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Abdominal aortic aneurysm (AAA) rupture is an important cause of death in older adults. In clinical practice, the most established predictor of AAA rupture is maximum AAA diameter. Aortic diameter is commonly used to assess AAA severity in mouse models studies. AAA rupture occurs when the stress (force per unit area) on the aneurysm wall exceeds wall strength. Previous research suggests that aortic wall structure and strength, biomechanical forces on the aorta and cellular and proteolytic composition of the AAA wall influence the risk of AAA rupture. Mouse models offer an opportunity to study the association of these factors with AAA rupture in a way not currently possible in patients. Such studies could provide data to support the use of novel surrogate markers of AAA rupture in patients. In this review, the currently available mouse models of AAA and their relevance to the study of AAA rupture are discussed. The review highlights the limitations of mouse models and suggests novel approaches that could be incorporated in future experimental AAA studies to generate clinically relevant results.

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Chronic cigarette smoke exposure triggers a vicious cycle of leukocyte and endothelial-mediated oxidant stress that results in vascular dysfunction

Cited by 35 publications

References 88 publications

Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase

Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase

Risk Factors for Recurrent Pancreatitis After First Episode of Acute Pancreatitis

Risk Factors and Mouse Models of Abdominal Aortic Aneurysm Rupture

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