Angiotensin-converting enzyme and subclinical atherosclerosis in psoriasis: Is there any association? A case-control study

Abdollahimajd, Fahimeh; Niknezhad, Nasim; Haghighatkhah, Hamid Reza; Namazi, Nastaran; Niknejad, Nakisa; Talebi, Atefeh

doi:10.1016/j.jaad.2018.08.003

Cited by 18 publications

(19 citation statements)

References 4 publications

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“…Our observations are in agreement with previous studies reporting an increase in subclinical atherosclerosis in Pso patients when compared to normal subjects [48][49][50][51].…”

Section: Discussionsupporting

confidence: 93%

The Oxidative Stress-Induced miR-200c Is Upregulated in Psoriasis and Correlates with Disease Severity and Determinants of Cardiovascular Risk

Magenta

D'agostino

Sileno

et al. 2019

Oxidative Medicine and Cellular Longevity

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Psoriasis is a chronic inflammatory skin disease associated with reactive oxygen species (ROS) increase and a higher risk of cardiovascular (CV) events. We previously showed that the miR-200 family (miR-200s) is induced by ROS, miR-200c being the most upregulated member responsible for apoptosis, senescence, ROS increase, and nitric oxide decrease, finally causing endothelial dysfunction. Moreover, circulating miR-200c increases in familial hypercholesterolemic children and in plaques and plasma of atherosclerotic patients, two pathologies associated with increased ROS. Given miR-200s’ role in endothelial dysfunction, ROS, and inflammation, we hypothesized that miR-200s were modulated in lesional skin (LS) and plasma of psoriatic patients (Pso) and that their levels correlated with some CV risk determinants at a subclinical level. All Pso had severe psoriasis, i.e., Psoriasis Area and Severity Index PASI>10, and one of the following: at least two systemic psoriasis treatments, age at onset<40 years, and disease duration>10 years. RNA was extracted from plasma (Pso, N=29; Ctrl, N=29) and from nonlesional skin (NLS) and LS of 6 Pso and 6 healthy subject skin (HS) biopsies. miR-200 levels were assayed by quantitative RT-PCR. We found that all miR-200s were increased in LS vs. NLS and miR-200c was the most expressed and upregulated in LS vs. HS. In addition, circulating miR-200c and miR-200a were upregulated in Pso vs. Ctrl. Further, miR-200c positively correlated with PASI, disease duration, left ventricular (LV) mass, LV relative wall thickness (RWT), and E/e′, a marker of diastolic dysfunction. Multiple regression analysis indicates a direct association between miR-200c and both RWT and LV mass. Circulating miR-200a correlated positively only with LV mass and arterial pressure augmentation index, a measure of stiffness, although the correlations were nearly significant (P=0.06). In conclusion, miR-200c is upregulated in LS and plasma of Pso, suggesting its role in ROS increase and inflammation associated with CV risk in psoriasis.

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“…Our observations are in agreement with previous studies reporting an increase in subclinical atherosclerosis in Pso patients when compared to normal subjects [48][49][50][51].…”

Section: Discussionsupporting

confidence: 93%

The Oxidative Stress-Induced miR-200c Is Upregulated in Psoriasis and Correlates with Disease Severity and Determinants of Cardiovascular Risk

Magenta

D'agostino

Sileno

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…Indeed, psoriasis is associated with a variety of comorbidities including metabolic syndrome, cardiovascular diseases (CVDs), inflammatory bowel diseases, and various other systemic conditions. [2][3][4][5][6][7][8][9][10] C-reactive protein (CRP) is a polypeptide and acute-phase reactant synthesized mainly by the hepatocytes during inflammation in response to certain cytokines, such as interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-α. [11][12][13][14] High-sensitivity CRP (hs-CRP) can show small changes in CRP levels during inflammation; therefore, it is a much more sensitive marker than CRP.…”

Section: Introductionmentioning

confidence: 99%

“…Regarding the fundamental role of systemic inflammation in the pathogenesis of psoriasis, it is no longer considered merely a skin disorder. Indeed, psoriasis is associated with a variety of comorbidities including metabolic syndrome, cardiovascular diseases (CVDs), inflammatory bowel diseases, and various other systemic conditions 2‐10 …”

Section: Introductionmentioning

confidence: 99%

High‐sensitivity C‐reactive protein as a biomarker in detecting subclinical atherosclerosis in psoriasis

Niknezhad

Haghighatkhah

Zargari

et al. 2020

Dermatologic Therapy

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Psoriasis is known to be associated with increased risk of cardiovascular diseases. High‐sensitivity C‐reactive protein (hs‐CRP) is a marker of inflammation and an independent risk factor for atherosclerosis. We aimed to assess the correlation between hs‐CRP and subclinical atherosclerosis in psoriatic patients. In 60 patients with moderate to severe psoriasis and 60 age‐ and gender matched healthy controls, we evaluated the serum hs‐CRP level and mean intima‐media thickness of the common carotid artery (MIMT‐CCA). Psoriatic patients had higher levels of hs‐CRP (median, 2.25 mg/L; IQR, 0.98‐3.80; and range, 0.29‐11.60) than did those in the control group (median, 1.03 mg/L; IQR, 0.36‐2.15; and range, 0.10‐3.35). Psoriatic patients also had higher mean MIMT (0.74 ± 0.19 and 0.54 ± 0.12, respectively, and P < .0001) compared with healthy subjects. The serum level of hs‐CRP was significantly correlated with MIMT (P < .0001). Our results indicate that psoriatic patients have a higher risk of subclinical atherosclerosis and hs‐CRP may be a useful marker for future risk of cardiovascular diseases in these patients. So, not only does anti‐inflammatory drugs play a key role in the treatment of psoriasis, but also they may reduce the risk of cardiovascular diseases by decreasing level of inflammatory markers including hs‐CRP.

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“…[76] An increase in serum ACE levels in patients with psoriasis has also repeatedly been reported. [77][78][79] The increase in tissue ACE in psoriasis seems to be disease specific and not present in other dermatoses with inflammatory component, [76] which makes it more likely that the increase in ACE is rather a driver and not a result of the pathology. However, a mechanism, by which increased ACE or Ang II levels may contribute to the pathogenesis of psoriasis, has not been identified.…”

Section: The Cutaneous Renin-angiotensin System and Psoriasismentioning

confidence: 99%

The role of the renin‐angiotensin system in skin physiology and pathophysiology

Silva

Assersen

Willadsen

et al. 2020

Experimental Dermatology

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From the early days until now, textbook knowledge and research about the renin-angiotensin system (RAS) have focused on the renal, vascular and central effects of the main effector hormone of the system, angiotensin II (Ang II). It is still widely unknown that all the RAS components are also expressed in skin, which is why working on the cutaneous RAS is sometimes like being caught between two stools: the scientific RAS community regards the skin as irrelevant as a target organ for the RAS and the dermatology/skin research community regards the RAS as irrelevant for skin physiology and pathophysiology. Despite this hindrance, the number of publications on the cutaneous RAS has steadily risen since the first description of the expression of all components of the RAS in rodent and human skin and is now in the hundreds. [1,2] These studies have provided strong evidence that the RAS is in fact

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Angiotensin-converting enzyme and subclinical atherosclerosis in psoriasis: Is there any association? A case-control study

Cited by 18 publications

References 4 publications

The Oxidative Stress-Induced miR-200c Is Upregulated in Psoriasis and Correlates with Disease Severity and Determinants of Cardiovascular Risk

The Oxidative Stress-Induced miR-200c Is Upregulated in Psoriasis and Correlates with Disease Severity and Determinants of Cardiovascular Risk

High‐sensitivity C‐reactive protein as a biomarker in detecting subclinical atherosclerosis in psoriasis

The role of the renin‐angiotensin system in skin physiology and pathophysiology

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