Role of monocytes/macrophages in renin-angiotensin system-induced hypertension and end organ damage

Barhoumi, Tlili; Todryk, Stephen

doi:10.3389/fphys.2023.1199934

Front. Physiol.

2023

DOI: 10.3389/fphys.2023.1199934

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Role of monocytes/macrophages in renin-angiotensin system-induced hypertension and end organ damage

Tlili Barhoumi,

Stephen Todryk

Abstract: Graphical AbstractRole of monocytes/macrophages in renin-angiotensin system-induced hypertension and end organ damage. RAS activation induces monocyte/macrophage pro-inflammatory-like phenotype polarization, directly and indirectly via cytokines (MCP-1, CCR2, IL-1b). Activation manifests in fibrosis, oxidative stress, endothelial dysfunction and low grade inflammation (IL-6, TNFa) and tus end organ damage. (HTA hypertension).

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2024

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Cited by 5 publications

References 71 publications

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Renal macrophages induce hypertension and kidney fibrosis in Angiotensin II salt mice model

Peter,

Umene,

et al. 2024

Biochemical and Biophysical Research Communications

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Renal macrophages induce hypertension and kidney fibrosis in Angiotensin II salt mice model

Peter,

Umene,

et al. 2024

Biochemical and Biophysical Research Communications

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Alamandine, a protective component of the renin-angiotensin system, reduces cellular proliferation and interleukin-6 secretion in human macrophages through MasR–MrgDR heteromerization

Rukavina Mikusic,

Silva,

Erra Díaz

et al. 2024

Biochemical Pharmacology

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Association of inflammatory and hematological indices with left ventricular hypertrophy in hypertensive patients

Pavlova,

Yasiukaits,

Barbuk

et al. 2024

Arter. gipertenz.

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Objective. To identify an associative relationship between inflammatory indicators, hematological indices and left ventricular hypertrophy (LVH) in patients with uncontrolled arterial hypertension (HTN). Design and methods. We examined 130 patients with uncomplicated essential HTN I–II with ineffective blood pressure (BP) control (≥ 140/90 mmHg). All patients underwent a clinical examination with determination of risk factors, indicators of inflammation — high-sensitivity C-reactive protein (hs-CRP), interleukin‑1β (IL‑1β), interleukin‑6 (IL‑6), interleukin‑8 (IL‑8), tumor necrosis factor α (TNF-α), hematological indices — systemic immune inflammation index (SII), the monocyte to high density lipoprotein cholesterol ratio (MHR), the platelet to lymphocyte ratio (PLR), the neutrophil to lymphocyte ratio (NLR), and echocardiography. Results. The positive correlations were found between the indicators of nonspecific inflammation and signs of LVH — MHR and left ventricular myocardial mass index (LVMI) (r = 0,448; p < 0,001), the posterior wall thickness (PWT) of left ventricle (LV) in the diastole (r = 0,256; p = 0,003), the interventricular septum (IVS) thickness in the diastole (r = 0,311; p ≤ 0,001); the level of hs-CRP and the relative wall thickness (RWT) (r = 0,283; p = 0,002), PWT of LV in the diastole (r = 0,202; p = 0,043), IVS thickness in the diastole (r = 0,231; p = 0,011); the level of IL‑6 and the PWT of LV in the diastole (r = 0,215; p = 0,018); SII and IVS thickness in the diastole (r = 0,230; p = 0,009), the RWT (r = 0,205; p = 0,016); NLR and IVS thickness in the diastole (r = 0,227; p = 0,009), PWT of LV in the diastole (r = 0,205; p = 0,029), RWT (r = 0,206; p = 0,016). Using multiple linear regression, independent factors associated with increased LVMI in HTN patients were male sex (β = 0,201), waist circumference (WC) (β = 0,258) and MHR (β = 0,236) (p = 0,029). Independent factors for increasing PWT of LV in the diastole in HTN patients were WC (β = 0,354) and male sex (β = 0,266) (p = 0,003); increase of IVS thickness in the diastole — SII (β = 0,254), WC (β = 0,392) and male sex (β = 0,219) (p = 0,021); and an increase of RWT — hs-CRP (β = 0,333) (p = 0,001). Conclusions. In patients with uncontrolled HTN increased levels of hs-CRP, IL‑6, SII, MHR and NLR were associated with echocardiographic LVH criteria—LVMI, PWT and IVS thickness in the diastole, RWT. Independent factors for increasing LVMI were WC, male sex and MHR; IVS thickness in the diastole — SII, WC and male; RWT — hs-CRP.

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Role of monocytes/macrophages in renin-angiotensin system-induced hypertension and end organ damage

Cited by 5 publications

References 71 publications

Renal macrophages induce hypertension and kidney fibrosis in Angiotensin II salt mice model

Renal macrophages induce hypertension and kidney fibrosis in Angiotensin II salt mice model

Alamandine, a protective component of the renin-angiotensin system, reduces cellular proliferation and interleukin-6 secretion in human macrophages through MasR–MrgDR heteromerization

Association of inflammatory and hematological indices with left ventricular hypertrophy in hypertensive patients

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