Cigarette smoke concentrate increases 8-epi-PGF2$alpha; and TGF$beta;1 secretion in rat mesangial cells

Mur, Cecilia; Clariá, J. J.; Rodela, S; Lario, Sergio; Campistol, J M; Titos, Esther; Íñigo, Pablo; Cases, A; Abián, Joaquín; Esmatjes, Enric

doi:10.1016/j.lfs.2003.12.026

Cited by 26 publications

(16 citation statements)

References 34 publications

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“…This study documented that nicotinic acetylcholine receptors, which mediate cell proliferation (49), are expressed on human mesangial cells. A study that used rat mesangial cells documented that exposition of these cells to cigarette smoke concentrate induced an increase of TGF-␤ 1 , a major player in the genesis of renal fibrosis, and 8-epi-PGF2␣, a marker of lipid peroxidation (50). Similar results were found in other experimental models and in humans (51)(52)(53).…”

Section: Nonhemodynamic Mechanisms As Potential Mediators Of Smoking-supporting

confidence: 65%

Smoking

Orth

Hallan²

2008

Clinical Journal of the American Society of Nephrology

254

174

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Although it is beyond any doubt that smoking is the number one preventable cause of death in most countries, smoking as an independent progression factor in renal disease has been questioned against the background of evidence-based criteria. This is because information from large, randomized, prospective studies that investigate the effects of smoking on renal function in healthy individuals as well as in patients with primary or secondary renal disease are lacking. Since 2003, a substantial number of clinical and experimental data concerning the adverse renal effects of smoking have been published, including large, prospective, population-based, observational studies. These more recent data together with evidence from experimental studies clearly indicate that smoking is a relevant risk factor, conferring a substantial increase in risk for renal function deterioration. This review summarizes the present knowledge about the renal risks of smoking as well as the increased cardiovascular risk caused by smoking in patients with chronic kidney disease. The conclusion is that smoking is an important renal risk factor, and nephrologists have to invest more efforts to motivate patients to stop smoking.

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Section: Nonhemodynamic Mechanisms As Potential Mediators Of Smoking-supporting

confidence: 65%

Smoking

Orth

Hallan²

2008

Clinical Journal of the American Society of Nephrology

254

174

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“…In addition, the PKC-␤-specific inhibitor LY379196 effectively prevented low density lipoprotein-induced PAI-1 production (54) as well as PAI-1 mRNA induction via ␣V␤3 (55). In models of diabetes, studies have shown that TGF-␤ mRNA expression can be modulated by a PKC-␤ specific inhibitor (33,34), and the induction of TGF-␤1 by cigarette smoke could be significantly suppressed by LY379196, suggesting PKC-␤ involvement (56). Our data now supply a possible link to these observations of PKC-␤ dependence via modulation of Smad6s.…”

Section: Discussionsupporting

confidence: 65%

Smad6s Regulates Plasminogen Activator Inhibitor-1 through a Protein Kinase C-β-dependent Up-regulation of Transforming Growth Factor-β

Berg¹,

Myers²,

Richardson

et al. 2005

Journal of Biological Chemistry

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“…Orth and Hallan [2] have extensively discussed possible mechanisms underlying the development of CKD in smokers, including heavy metal toxicity due to inhalation of tobacco smoke [20][21][22], intrarenal vasoconstriction [23][24][25][26][27], and oxidative stress and the inflammatory process [28][29][30]. Based on the relatively copious body of evidence from previous studies, glomerular hypertension due to intrarenal vasoconstriction seems the most plausible mechanism, which is in turn related to a stimulated renin-angiotensin-aldosterone system (RAAS) caused by the nicotine inhaled with the cigarette smoke.…”

Section: The Risk Of Low Gfr In Smokersmentioning

confidence: 99%

The effects of continuing and discontinuing smoking on the development of chronic kidney disease (CKD) in the healthy middle-aged working population in Japan

Noborisaka

Ishizaki

Yamada

et al. 2012

Environ Health Prev Med

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Objectives The strength of the association between smoking and the development of chronic kidney disease (CKD) in the healthy middle-aged working age population has not been established. Methods This was a retrospective 6-year observational study involving 4,121 male and 2,877 female workers who were free of primary kidney disease, diabetes mellitus, severe hypertension, and the signs and symptoms of CKD. Proteinuria was detected by a dipstick method, and glomerular filtration rate (GFR) was estimated by the equation of the Japan Society of Nephrology. Results Sixty men (1.5 %) and 21 women (0.7 %) developed proteinuria over the 6 years of the study. Irrespective of sex, in comparison with non-smokers, those who continued smoking showed an odds ratio (OR) of 2.52 with a 95 % confidence interval (CI) of 1.50-4.25 for developing proteinuria while those who quit smoking showed an OR of 1.29 (95 % CI 0.48-3.42), following adjustment for confounders. Among the study population, 443 men (10.7 %) and 356 women (12.4 %) developed a GFR of \60 mL/min/1.73 m 2 , corresponding to stage III CKD. Continuing smokers had a low OR (0.74, 95 % CI 0.60-0.90) for developing a low GFR, as well as a higher mean GFR than non-smokers. The reduction in GFR during the 6-year study period was not different between smokers and non-smokers, but it was larger in those who developed proteinuria than in those who did not, irrespective of smoking.Conclusions Continuing smokers showed a twofold or more higher risk of developing proteinuria. Discontinuation of smoking substantially reduced the risk. A longer observational period may be required to detect the smoking-induced risk of developing stage III CKD in the middle-aged working population.

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Cigarette smoke concentrate increases 8-epi-PGF2$alpha; and TGF$beta;1 secretion in rat mesangial cells

Cited by 26 publications

References 34 publications

Smoking

Smoking

Smad6s Regulates Plasminogen Activator Inhibitor-1 through a Protein Kinase C-β-dependent Up-regulation of Transforming Growth Factor-β

The effects of continuing and discontinuing smoking on the development of chronic kidney disease (CKD) in the healthy middle-aged working population in Japan

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