Renin-angiotensin system and inflammation update

Cantero-Navarro, Elena; Fernández-Fernández, Beatriz; Ramos, Adrián M.; Rayego‐Mateos, Sandra; Rodrigues-Díez, Raúl R.; Sánchez-Niño, María D.; Sanz, Ana B.; Ruíz-Ortega, Marta; Ortíz, Alberto

doi:10.1016/j.mce.2021.111254

Cited by 57 publications

(35 citation statements)

References 182 publications

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Section: Discussionmentioning

confidence: 99%

“…Ac-SDKP is an anti-inflammatory tetrapeptide released from thymosin-β4 by the sequential action of meprin-α and prolyl oligopeptidase (POP), and it is cleaved by angiotensin-converting enzyme (ACE) [ 29 ]. In preclinical studies, Ac-SDKP protected from a wide range of lung, kidney, and cardiovascular injury models and demonstrated anti-inflammatory properties, decreasing the infiltration by macrophages and neutrophils, nuclear factor kappa-B (NF-κB) activation or inflammatory molecules, as well as antifibrotic effects [ 29 ]. Studies have shown that the anti-fibrosis properties of Ac-SDKP are partly mediated by its anti-inflammatory activity, i.e., inhibiting the differentiation of bone marrow stem cells to macrophages, the activation and migration of macrophages, inflammatory signaling pathways, and the release of cytokines [ 30 , 31 , 32 ].…”

Section: Discussionmentioning

confidence: 99%

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Glycolytic Reprogramming in Silica-Induced Lung Macrophages and Silicosis Reversed by Ac-SDKP Treatment

Mao

Yang

Yin

et al. 2021

IJMS

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Glycolytic reprogramming is an important metabolic feature in the development of pulmonary fibrosis. However, the specific mechanism of glycolysis in silicosis is still not clear. In this study, silicotic models and silica-induced macrophage were used to elucidate the mechanism of glycolysis induced by silica. Expression levels of the key enzymes in glycolysis and macrophage activation indicators were analyzed by Western blot, qRT-PCR, IHC, and IF analyses, and by using a lactate assay kit. We found that silica promotes the expression of the key glycolysis enzymes HK2, PKM2, LDHA, and macrophage activation factors iNOS, TNF-α, Arg-1, IL-10, and MCP1 in silicotic rats and silica-induced NR8383 macrophages. The enhancement of glycolysis and macrophage activation induced by silica was reduced by Ac-SDKP or siRNA-Ldha treatment. This study suggests that Ac-SDKP treatment can inhibit glycolytic reprogramming in silica-induced lung macrophages and silicosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Glycolytic Reprogramming in Silica-Induced Lung Macrophages and Silicosis Reversed by Ac-SDKP Treatment

Mao

Yang

Yin

et al. 2021

IJMS

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“…Furthermore, they may potentially modulate responses of Th17 and Treg lymphocytes. Furthermore, they also regulate Klotho and other anti-inflammatory factors [ 69 ].…”

Section: Vra and Egfr Reductionmentioning

confidence: 99%

A Shared Nephroprotective Mechanism for Renin-Angiotensin-System Inhibitors, Sodium-Glucose Co-Transporter 2 Inhibitors, and Vasopressin Receptor Antagonists: Immunology Meets Hemodynamics

Capolongo

Capasso

Viggiano

2022

IJMS

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A major paradigm in nephrology states that the loss of filtration function over a long time is driven by a persistent hyperfiltration state of surviving nephrons. This hyperfiltration may derive from circulating immunological factors. However, some clue about the hemodynamic effects of these factors derives from the effects of so-called nephroprotective drugs. Thirty years after the introduction of Renin-Angiotensin-system inhibitors (RASi) into clinical practice, two new families of nephroprotective drugs have been identified: the sodium-glucose cotransporter 2 inhibitors (SGLT2i) and the vasopressin receptor antagonists (VRA). Even though the molecular targets of the three-drug classes are very different, they share the reduction in the glomerular filtration rate (GFR) at the beginning of the therapy, which is usually considered an adverse effect. Therefore, we hypothesize that acute GFR decline is a prerequisite to obtaining nephroprotection with all these drugs. In this study, we reanalyze evidence that RASi, SGLT2i, and VRA reduce the eGFR at the onset of therapy. Afterward, we evaluate whether the extent of eGFR reduction correlates with their long-term efficacy. The results suggest that the extent of initial eGFR decline predicts the nephroprotective efficacy in the long run. Therefore, we propose that RASi, SGLT2i, and VRA delay kidney disease progression by controlling maladaptive glomerular hyperfiltration resulting from circulating immunological factors. Further studies are needed to verify their combined effects.

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“…ACE-2 cleaves Ang II to Ang (1–7) and exerts vasodilatation, anti-inflammation, and anti-fibrotic effects by Mas receptor system activation. RAAS activation effects depend on the tissue ACE/ACE2 balance, which could be affected by several factors [ 44 , 45 , 46 ].…”

Section: Pathophysiological Mechanisms Of Sars-cov-2 and Its Neurological Implicationsmentioning

confidence: 99%

Use of Antioxidants for the Neuro-Therapeutic Management of COVID-19

et al. 2021

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Coronavirus Disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), is an emergent infectious disease that has caused millions of deaths throughout the world. COVID-19 infection’s main symptoms are fever, cough, fatigue, and neurological manifestations such as headache, myalgias, anosmia, ageusia, impaired consciousness, seizures, and even neuromuscular junctions’ disorders. In addition, it is known that this disease causes a series of systemic complications such as adverse respiratory distress syndrome, cardiac injury, acute kidney injury, and liver dysfunction. Due to the neurological symptoms associated with COVID-19, damage in the central nervous system has been suggested as well as the neuroinvasive potential of SARS-CoV-2. It is known that CoV infections are associated with an inflammation process related to the imbalance of the antioxidant system; cellular changes caused by oxidative stress contribute to brain tissue damage. Although anti-COVID-19 vaccines are under development, there is no specific treatment for COVID-19 and its clinical manifestations and complications; only supportive treatments with immunomodulators, anti-vascular endothelial growth factors, modulating drugs, statins, or nutritional supplements have been used. In the present work, we analyzed the potential of antioxidants as adjuvants for the treatment of COVID-19 and specifically their possible role in preventing or decreasing the neurological manifestations and neurological complications present in the disease.

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Renin-angiotensin system and inflammation update

Cited by 57 publications

References 182 publications

Glycolytic Reprogramming in Silica-Induced Lung Macrophages and Silicosis Reversed by Ac-SDKP Treatment

Glycolytic Reprogramming in Silica-Induced Lung Macrophages and Silicosis Reversed by Ac-SDKP Treatment

A Shared Nephroprotective Mechanism for Renin-Angiotensin-System Inhibitors, Sodium-Glucose Co-Transporter 2 Inhibitors, and Vasopressin Receptor Antagonists: Immunology Meets Hemodynamics

Use of Antioxidants for the Neuro-Therapeutic Management of COVID-19

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