Table 2.
Studies related to salt-induced inflammation in renal failure models.
| Year | Model | Findings | Refs |
|---|---|---|---|
| 2011 | Subtotal nephrectomized rats treated with NaCl drinking water | NaCl-loaded subtotal nephrectomy caused LVH, hypertension, and increased plasma levels of PTH, creatinine, inorganic phosphorus, ADMA, and IL-6. | [71] |
| 2013 | 5/6 nephrectomized rats with nitric oxide depletion and a high-salt diet | Renal failure developed by 12 weeks after subtotal nephrectomy. Inflammation-related tubulo-interstitial damage and fibrosis, tubular atrophy, and focal glomerulosclerosis led to massive reduction of healthy glomeruli within the remnant kidney. | [72] |
| 2015 | 5/6 nephrectomized rats with high-salt diet | High salt activated the intrarenal and cerebral renin-angiotensin axes, which is related to the promotion of oxidative stress, renal fibrosis, and progression of CKD. | [73] |
| 2017 | 5/6 nephrectomized mice with salt loading | Salt loading induced macrophage infiltration in the peritoneal wall, heart, and para-aortic tissues through the TonEBP–MCP-1 pathway. | [50] |
| 2019 | 5/6 nephrectomized mice with salt loading | Salt loading induced peritoneal inflammation, angiogenesis, and high peritoneal transport rate. Blockade of IL-6 signaling rescued peritoneal transport function. | [74] |
| 2020 | Rats treated with nitric oxide synthase inhibition and a high-salt diet | Early treatment with NF-κB inhibitor prevented the development of late renal injury and inflammation. | [75] |
| 2021 | High-salt-load 5/6 nephrectomized rats | Inhibition of central PRR expression reduced inflammation and oxidative stress in both brain and kidney and ameliorated renal injury and fibrosis. The central MAPK/ERK1/2 and PI3K/Akt signaling pathways were related to the mechanism as well as the angiotensin-converting enzyme 1–angiotensin II–angiotensin type 1 receptors axis. | [76] |
| 2021 | 5/6 nephrectomized rats with NaCl treatment | NaCl treatment induced a pro-inflammatory phenotype in peritoneal macrophages derived from nephrectomized rats. High salt intake promoted immune activation of macrophages through phosphorylation of STAT1. | [77] |
| 2022 | 5/6 nephrectomized mice with salt loading | Salt loading induced cardiac inflammation and fibrosis along with elevated levels of proinflammatory cytokines. Blockade of IL-6 signaling showed anti-inflammatory, antifibrotic, and partial antioxidative effects on the heart. | [78] |
Abbreviations: left ventricular hypertrophy (LVH), parathyroid hormone (PTH), asymmetric dimethylarginine (ADMA), interleukin-6 (IL-6), chronic kidney disease (CKD), tonicity-responsive enhancer binding protein (TonEBP), monocyte chemotactic protein-1 (MCP-1), nuclear factor-kappa B (NF-κB), (Pro)renin receptor (PRR), mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), phosphatidylinositol-3 kinase (PI3K), signal transducer and activator of transcription 1 (STAT1).