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Renin–Angiotensin–Aldosterone System and Immunomodulation: a State-Of-The-Art Review

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Renin–Angiotensin–Aldosterone System and Immunomodulation: a State-Of-The-Art Review cells Review Renin–Angiotensin–Aldosterone System and Immunomodulation: A State-of-the-Art Review Driss Laghlam , Mathieu Jozwiak and Lee S. Nguyen * Research and Innovation of CMC Ambroise Paré (RICAP), CMC Ambroise Paré, 25-27 Boulevard Victor Hugo, 92200 Neuilly-sur-Seine, France; [email protected] (D.L.); [email protected] (M.J.) * Correspondence: [email protected] Abstract: The renin–angiotensin system (RAS) has long been described in the field of cardiovascular physiology as the main player in blood pressure homeostasis. However, other effects have since been described, and include proliferation, fibrosis, and inflammation. To illustrate the immunomodulatory properties of the RAS, we chose three distinct fields in which RAS may play a critical role and be the subject of specific treatments. In oncology, RAS hyperactivation has been associated with tumor migration, survival, cell proliferation, and angiogenesis; preliminary data showed promise of the benefit of RAS blockers in patients treated for certain types of cancer. In intensive care medicine, vasoplegic shock has been associated with severe macro- and microcirculatory imbalance. A relative insufficiency in angiotensin II (AngII) was associated to lethal outcomes and synthetic AngII has been suggested as a specific treatment in these cases. Finally, in solid organ transplantation, both AngI and AngII have been associated with increased rejection events, with a regional specificity in the RAS activity. These elements emphasize the complexity of the direct and indirect interactions of RAS with immunomodulatory pathways and warrant further research in the field. Keywords: renin–angiotensin system; oncology; shock; transplantation; immunomodulation Citation: Laghlam, D.; Jozwiak, M.; Nguyen, L.S. Renin–Angiotensin– Aldosterone System and Immunomodulation: A State-of- 1. Introduction the-Art Review. Cells 2021, 10, 1767. The renin–angiotensin system (RAS) has long been considered the pinnacle of home- https://doi.org/10.3390/cells10071767 ostasis in cardiovascular physiology. Its main function involves regulation of blood pres- Academic Editor: András Balla sure, via direct and indirect means, through electrolyte balance, and trophic and vasomotor functions. While historically associated with these basic functions, the role of inflammation Received: 9 May 2021 in cardiovascular diseases has been more and more described, and a critical role of RAS in Accepted: 9 July 2021 inflammation regulation has been suggested. Published: 13 July 2021 Using three different fields of application, we hereafter describe non-classical RAS functions, relying on the immunomodulatory features of RAS: oncology, intensive care, Publisher’s Note: MDPI stays neutral and transplantation (see Figure1). with regard to jurisdictional claims in published maps and institutional affil- iations. Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/). Cells 2021, 10, 1767. https://doi.org/10.3390/cells10071767 https://www.mdpi.com/journal/cells Cells 2021, 10, x 1767 FOR PEER REVIEW 2 2of of 27 28 Figure 1. 1. EffectsEffects of of the the renin–angiotensin renin–angiotensin system system (RAS) (RAS) and and its its featur featureses in in oncology, oncology, vasoplegic vasoplegic shock, shock, and and transplantation. transplantation. Abbreviations: AngI: angiotensin I, AngII: angiotensin II. 2.2. Part Part 1: 1: Renin–Angiotensin Renin–Angiotensin System System Blockers Blockers and and Malignancies Malignancies Renin–angiotensinRenin–angiotensin system system blockers blockers (RASBs (RASBs),), which include angiotensin-converting enzymeenzyme inhibitors inhibitors (ACEIs) (ACEIs) and and angiotensin-2 angiotensin-2 re receptorceptor 1 1 blockers blockers (ARB (ARBs),s), have been used asas antihypertensive antihypertensive drugs drugs for for several several decades, decades, showing showing benefits benefits in terms terms of morbidity morbidity and and mortalitymortality in in cardiovascular cardiovascular diseases. diseases. OnlyOnly recently havehave other other organ-protective organ-protective effects effects been been described. described. These These encompassed encom- passedinhibition inhibition of cardiac of cardiac hypertrophy, hypertrophy, remodeling, remodeling, fibrosis, fibrosis, and reactive and oxygenreactive species oxygen (ROS) spe- ciesproduction. (ROS) production. Notably, numerous Notably, numerous observations obse ofrvations RASB treatments of RASB treatments in patients in with patients solid withcancers solid showed cancers some showed benefits, some even benefits, towards even survival towards that survival was free that of cancer was free evolution. of cancer In evolution.the following In the section, following we describe section, thewe interactionsdescribe the betweeninteractions RAS between and cancer. RAS and cancer. 2.1.2.1. Pathways Pathways Related Related to to RAS RAS AngiotensinogenAngiotensinogen (synthesized (synthesized in in the the liver) liver) is is the the only only precursor precursor protein protein of RAS and thethe source source of of all all angiotensin angiotensin peptides. peptides. Angiot Angiotensinogenensinogen is primarily is primarily cleaved cleaved in blood in blood cir- culationcirculation by byrenin renin (protease (protease sy synthesizednthesized in in the the kidney), kidney), to to angiotensin angiotensin I I(AngI), (AngI), which which in turnturn is processed byby angiotensinangiotensin converting converting enzyme enzyme (ACE) (ACE) (secreted (secreted in lung)in lung) to produceto produce the theactive active octapeptide, octapeptide, angiotensin angiotensin II (AngII). II (Ang AngIIII). actions AngII are actions primary are mediated primary through mediated the throughbinding ofthe its binding two receptors, of its two type receptors, 1 (AT1R) type and type1 (AT1R) 2 (AT2R), and whichtype 2 belong(AT2R), to which the G protein-belong tocoupled the G protein-coupled receptor superfamily. receptor The superfamily important cardiovascular. The important actions cardiovascular of AngII, actions including of AngII,regulation including of arterial regulation blood pressure of arterial with blood short-term pressure vasoconstriction, with short-term aldosterone vasoconstriction, release, aldosteroneand water and release, salt balance, and water are and predominantly salt balance, mediated are predominantly by AT1R in mediated target tissues, by AT1R such in as targetblood tissues, vessels, such kidney, as blood brain, vessels, and heart kidney, [1]. brain, and heart [1]. On the other hand, increasing evidence supports the concept of a counter regulatory renin–angiotensin system with opposite effects in cardiovascular physiology and disease Cells 2021, 10, 1767 3 of 28 Cells 2021, 10, x FOR PEER REVIEW 3 of 27 On the other hand, increasing evidence supports the concept of a counter regulatory renin–angiotensin system with opposite effects in cardiovascular physiology and disease [2]. [2].Angiotensin Angiotensin converting converting enzyme enzyme 1 (ACE2) 1 (ACE2) and and neprilysin neprilysin (NEP) (NEP) are are part part of of this this counter coun- terregulatory regulatory system. system. ACE2 ACE2 and and NEP NEP can can cleave clea AngIIve AngII to produce to produce angiotensin angiotensin 1–7 (Ang1–7 (Ang 1–7), 1–7),and ACE2and ACE2 cleaves cleaves AngI AngI to generate to generate angiotensin angiotensin 1–9 (Ang1–9 (Ang 1–9) 1–9) (see Figure(see Figure2). These 2). These two twopeptides peptides mediate mediate the the antagonistic antagonistic effects effects of of AngII. AngII. Angiotensin Angiotensin 1–7 1–7 bindsbinds toto the proto- proto- oncogenoncogen Mas Mas receptor, receptor, which which leads leads to to vasodila vasodilation,tion, antihypertensive, antihypertensive, and and antifibrosis antifibrosis ef- fectseffects [3], [3 while], while Ang Ang 1–9 1–9 can can activate activate AT2R AT2R to to trigger trigger natriuresis natriuresis and and NO NO production, production, thus thus mediatingmediating vasodilatory effects an andd reducing blood pressure [[4].4]. Figure 2. Renin–angiotensinRenin–angiotensin system: system: classical classical and and counter counter regulato regulatoryry pathways. pathways. Abbreviations: Abbreviations: ACE: ACE: angiotensin angiotensin convert- con- ing enzyme; ACE 2: angiotensin-converting enzyme type 2, ACEIs: angiotensin-converting enzyme inhibitors; ARBs: an- verting enzyme; ACE 2: angiotensin-converting enzyme type 2, ACEIs: angiotensin-converting enzyme inhibitors; ARBs: giotensin-2 receptor 1 blockers, AT1R: angiotensin II receptor type1, AT2R: angiotensin II receptor type 2. angiotensin-2 receptor 1 blockers, AT1R: angiotensin II receptor type1, AT2R: angiotensin II receptor type 2. OverOver the the past decade, growing evidence ha hass shown that an altered immune system isis likely likely to to be be a a key contributor to the deve developmentlopment of hypertension. Consistent evidence demonstratesdemonstrates that that various various immune immune cell cell subsets subsets infiltrate infiltrate blood vessels, kidneys, heart, heart, and/orand/or the the autonomic autonomic nervous systemsystem duringduring hypertension, hypertension, and and that that the the targeted targeted depletion deple- tionof specific of specific immune immune cell subsets cell subsets or inhibition
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