Cardiovascular effect of inflammation and nonsteroidal anti-inflammatory drugs on renin–angiotensin system in experimental arthritis

Asghar, Waheed; Aghazadeh‐Habashi, Ali; Jamali, Fakhreddin

doi:10.1007/s10787-017-0344-1

Cited by 25 publications

(20 citation statements)

References 36 publications

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“…In this study, Wistar rats that received exclusively meloxicam showed renal histological changes (basal membrane thickening and tubulointerstitial nephritis), which are in agreement with other studies [32][33][34] . On the other hand, rats that received meloxicam associated with nitrosyl ruthenium did not present such histological alterations and this is our main result.…”

Section: ■ Discussionsupporting

confidence: 93%

New metallophamaceutic reduced renal injury induced by non-steroidal anti-inflammatory

et al. 2019

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Section: ■ Discussionsupporting

confidence: 93%

New metallophamaceutic reduced renal injury induced by non-steroidal anti-inflammatory

et al. 2019

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“…Examples of potential mechanisms of cardiac injury from COVID-19 include damage to the microvascular structure, ischemia from low oxygen availability, immune response-related inflammatory syndrome, and direct viral infection of the heart (11,(37)(38)(39)(40). From previous non-COVID-19 studies, it is known that inflammation can negatively affect cardiovascular health through actuating the reninangiotensin system (RAS) and thus disturbing the homeostasis of vasodilator and vasoconstrictor angiotensin peptides in the heart (41,42). Since both TnI and CK-MB are structural cardiac proteins, the severity of COVID-19 infection will determine the intensity of changes in these cardiac-specific markers.…”

Section: Discussionmentioning

confidence: 99%

Assessing the Elevation of Cardiac Biomarkers and the Severity of COVID-19 Infection: A Meta-analysis

Walker

Deb²,

Ling³

et al. 2020

J Pharm Pharm Sci

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- Purpose: Since December 2019, coronavirus disease 2019 infection has become a global pandemic. The cases of Coronavirus Disease 2019 (COVID-19)-related acute cardiac injury with unknown pathophysiologic mechanism has become increasingly prevalent. However, it is not yet understood how the extent of cardiac injury differs with the intensity of viral infection. In the current study, we aimed to assess the association between elevated cardiac biomarkers and the severity of COVID-19 infection. Methods: A systematic literature search was performed across PubMed and Embase databases from December 1, 2019 to July 10, 2020, to identify studies that reported cardiac biomarkers of troponin (TnI) and creatine kinase-myocardial band (CK-MB) in patients with COVID-19. These studies compared non-severe patients with severe patients, or survivors with non-survivors or medical patients with critically ill patients. The data were extracted for TnI, CK-MB, N-terminal-brain natriuretic peptide (NT-BNP), D-dimer, and lactate dehydrogenase (LDH), C-reactive protein (CRP), and interleukin 6 (IL-6). Wherever possible, the data were pooled for meta-analysis (Review Manager, RevMan. version 5.3) with standard or weighted mean or median difference and corresponding 95% confidence intervals (95% CI). Results: A total of 25 studies involving 5,626 patients were included in the present analysis. More severe COVID-19 infection was found to be associated with higher mean values of TnI (-0.54 [-0.72, -0.36]) (ng/mL), CK-MB (-1.55 [-2.23, -0.88]) (ng/mL) and (-4.75 [-13.31, 3.82]) (units/L), NT-BNP (-815.7 [-1073.97, -557.42]) (pg/mL), D-dimer (-1.4 [-2.04, -0.77]) (mcg/mL), and LDH (-176.59 [-224.11, -129.06]) (units/L), as well as CRP (-64.03 [-68.88, -59.19]) (mg/L) and IL-6 (-22.59 [-29.39, -15.79]) (pg/mL). Conclusions: There is significant association between elevated cardiac biomarkers and the severity of COVID-19, which underlines the increased risk of acute cardiac injury with more severe viral infection. This highlights the need to understand the cardiac history among the COVID-19 patients during initial assessment and for monitoring.

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“…Ibuprofen, a commonly used NSAID and non-selective COX inhibitor, attenuates cardiac fibrosis and upregulates cardiac ACE2 expression in streptozotocin-induced diabetic rats ( Qiao et al, 2015 ). Other NSAIDs, including rofecoxib, meloxicam, celecoxib and flurbiprofen, at clinically relevant doses, were shown to induce modest increases in renal and cardiac ACE2 protein expression in adjuvant-induced arthritic rats ( Asghar, Aghazadeh-Habashi, & Jamali, 2017 ).…”

Section: Corticosteroids Non-steroid Anti-inflammatory Drugs and Acmentioning

confidence: 99%

A comprehensive guide to the pharmacologic regulation of angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 entry receptor

Öz

Lorke

Kabbani

2021

Pharmacology & Therapeutics

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The recent emergence of coronavirus disease-2019 (COVID-19) as a global pandemic has prompted scientists to address an urgent need for defining mechanisms of disease pathology and treatment. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent for COVID-19, employs angiotensin converting enzyme 2 (ACE2) as its primary target for cell surface attachment and likely entry into the host cell. Thus, understanding factors that may regulate the expression and function of ACE2 in the healthy and diseased body is critical for clinical intervention. Over 66% of all adults in the United States are currently using a prescription drug and while earlier findings have focused on possible upregulation of ACE2 expression through the use of renin angiotensin system (RAS) inhibitors, mounting evidence suggests that various other widely administered drugs used in the treatment of hypertension, heart failure, diabetes mellitus, hyperlipidemias, coagulation disorders, and pulmonary disease may also present a varied risk for COVID-19. Specifically, we summarize mechanisms on how heparin, statins, steroids and phytochemicals, besides their established therapeutic effects, may also interfere with SARS-CoV-2 viral entry into cells. We also describe evidence on the effect of several vitamins, phytochemicals, and naturally occurring compounds on ACE2 expression and activity in various tissues and disease models. This comprehensive review aims to provide a timely compendium on the potential impact of commonly prescribed drugs and pharmacologically active compounds on COVID-19 pathology and risk through regulation of ACE2 and RAS signaling.

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Cardiovascular effect of inflammation and nonsteroidal anti-inflammatory drugs on renin–angiotensin system in experimental arthritis

Cited by 25 publications

References 36 publications

New metallophamaceutic reduced renal injury induced by non-steroidal anti-inflammatory

New metallophamaceutic reduced renal injury induced by non-steroidal anti-inflammatory

Assessing the Elevation of Cardiac Biomarkers and the Severity of COVID-19 Infection: A Meta-analysis

A comprehensive guide to the pharmacologic regulation of angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 entry receptor

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