Accumulation of Renal Fibrosis in Hyperuricemia Rats Is Attributed to the Recruitment of Mast Cells, Activation of the TGF-β1/Smad2/3 Pathway, and Aggravation of Oxidative Stress
Renal fibrosis is relentlessly progressive and irreversible, and a life-threatening risk. With the continuous intake of a high-purine diet, hyperuricemia has become a health risk factor in addition to hyperglycemia, hypertension, and hyperlipidemia. Hyperuricemia is also an independent risk factor f...
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| Veröffentlicht in: | International journal of molecular sciences 2023-06, Vol.24 (13), p.10839 |
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| creator | Zhang, Mingkang Cui, Ruirui Zhou, Yan Ma, Yanrong Jin, Yongwen Wang, Lina Kou, Wen Wu, Xin'an |
| description | Renal fibrosis is relentlessly progressive and irreversible, and a life-threatening risk. With the continuous intake of a high-purine diet, hyperuricemia has become a health risk factor in addition to hyperglycemia, hypertension, and hyperlipidemia. Hyperuricemia is also an independent risk factor for renal interstitial fibrosis. Numerous studies have reported that increased mast cells (MCs) are closely associated with kidney injury induced by different triggering factors. This study investigated the effect of MCs on renal injury in rats caused by hyperuricemia and the relationship between MCs and renal fibrosis. Our results reveal that hyperuricemia contributes to renal injury, with a significant increase in renal MCs, leading to renal fibrosis, mitochondrial structural disorders, and oxidative stress damage. The administration of the MCs membrane stabilizer, sodium cromoglycate (SCG), decreased the expression of SCF/c-kit, reduced the expression of α-SMA, MMP2, and inhibited the TGF-β1/Smad2/3 pathway, thereby alleviating renal fibrosis. Additionally, SCG reduced renal oxidative stress and mitigated mitochondrial structural damage by inhibiting Ang II production and increasing renal GSH, GSH-Px, and GR levels. Collectively, the recruitment of MCs, activation of the TGF-β1/Smad2/3 pathway, and Ang II production drive renal oxidative stress, ultimately promoting the progression of renal fibrosis in hyperuricemic rats. |
| doi_str_mv | 10.3390/ijms241310839 |
| format | Article |
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With the continuous intake of a high-purine diet, hyperuricemia has become a health risk factor in addition to hyperglycemia, hypertension, and hyperlipidemia. Hyperuricemia is also an independent risk factor for renal interstitial fibrosis. Numerous studies have reported that increased mast cells (MCs) are closely associated with kidney injury induced by different triggering factors. This study investigated the effect of MCs on renal injury in rats caused by hyperuricemia and the relationship between MCs and renal fibrosis. Our results reveal that hyperuricemia contributes to renal injury, with a significant increase in renal MCs, leading to renal fibrosis, mitochondrial structural disorders, and oxidative stress damage. The administration of the MCs membrane stabilizer, sodium cromoglycate (SCG), decreased the expression of SCF/c-kit, reduced the expression of α-SMA, MMP2, and inhibited the TGF-β1/Smad2/3 pathway, thereby alleviating renal fibrosis. Additionally, SCG reduced renal oxidative stress and mitigated mitochondrial structural damage by inhibiting Ang II production and increasing renal GSH, GSH-Px, and GR levels. Collectively, the recruitment of MCs, activation of the TGF-β1/Smad2/3 pathway, and Ang II production drive renal oxidative stress, ultimately promoting the progression of renal fibrosis in hyperuricemic rats.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms241310839</identifier><identifier>PMID: 37446016</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adefovir dipivoxil ; Angiotensin II ; Animals ; c-Kit protein ; Cell activation ; Creatinine ; Diet ; Fibrosis ; Gelatinase A ; Health aspects ; Histopathology ; Hyperglycemia ; Hyperlipidemia ; Hypertension ; Hyperuricemia ; Hyperuricemia - metabolism ; Kidney - metabolism ; Kidney diseases ; Kidney Diseases - metabolism ; Mast cells ; Mast Cells - metabolism ; Oxidation ; Oxidative Stress ; Rats ; Risk factors ; Signal Transduction ; Smad2 protein ; Sodium cromoglycate ; Transforming Growth Factor beta1 - metabolism ; Transforming growth factor-b1 ; Transforming growth factors ; Uric acid ; Valsartan</subject><ispartof>International journal of molecular sciences, 2023-06, Vol.24 (13), p.10839</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 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/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-fa139ad5b44e0d3aaf8e61eea37a6556073fabd0dee0778e457e92cf0bf8eb5e3</citedby><cites>FETCH-LOGICAL-c483t-fa139ad5b44e0d3aaf8e61eea37a6556073fabd0dee0778e457e92cf0bf8eb5e3</cites><orcidid>0000-0002-0371-0361</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10341566/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10341566/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37446016$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Mingkang</creatorcontrib><creatorcontrib>Cui, Ruirui</creatorcontrib><creatorcontrib>Zhou, Yan</creatorcontrib><creatorcontrib>Ma, Yanrong</creatorcontrib><creatorcontrib>Jin, Yongwen</creatorcontrib><creatorcontrib>Wang, Lina</creatorcontrib><creatorcontrib>Kou, Wen</creatorcontrib><creatorcontrib>Wu, Xin'an</creatorcontrib><title>Accumulation of Renal Fibrosis in Hyperuricemia Rats Is Attributed to the Recruitment of Mast Cells, Activation of the TGF-β1/Smad2/3 Pathway, and Aggravation of Oxidative Stress</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Renal fibrosis is relentlessly progressive and irreversible, and a life-threatening risk. With the continuous intake of a high-purine diet, hyperuricemia has become a health risk factor in addition to hyperglycemia, hypertension, and hyperlipidemia. Hyperuricemia is also an independent risk factor for renal interstitial fibrosis. Numerous studies have reported that increased mast cells (MCs) are closely associated with kidney injury induced by different triggering factors. This study investigated the effect of MCs on renal injury in rats caused by hyperuricemia and the relationship between MCs and renal fibrosis. Our results reveal that hyperuricemia contributes to renal injury, with a significant increase in renal MCs, leading to renal fibrosis, mitochondrial structural disorders, and oxidative stress damage. The administration of the MCs membrane stabilizer, sodium cromoglycate (SCG), decreased the expression of SCF/c-kit, reduced the expression of α-SMA, MMP2, and inhibited the TGF-β1/Smad2/3 pathway, thereby alleviating renal fibrosis. 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With the continuous intake of a high-purine diet, hyperuricemia has become a health risk factor in addition to hyperglycemia, hypertension, and hyperlipidemia. Hyperuricemia is also an independent risk factor for renal interstitial fibrosis. Numerous studies have reported that increased mast cells (MCs) are closely associated with kidney injury induced by different triggering factors. This study investigated the effect of MCs on renal injury in rats caused by hyperuricemia and the relationship between MCs and renal fibrosis. Our results reveal that hyperuricemia contributes to renal injury, with a significant increase in renal MCs, leading to renal fibrosis, mitochondrial structural disorders, and oxidative stress damage. The administration of the MCs membrane stabilizer, sodium cromoglycate (SCG), decreased the expression of SCF/c-kit, reduced the expression of α-SMA, MMP2, and inhibited the TGF-β1/Smad2/3 pathway, thereby alleviating renal fibrosis. Additionally, SCG reduced renal oxidative stress and mitigated mitochondrial structural damage by inhibiting Ang II production and increasing renal GSH, GSH-Px, and GR levels. Collectively, the recruitment of MCs, activation of the TGF-β1/Smad2/3 pathway, and Ang II production drive renal oxidative stress, ultimately promoting the progression of renal fibrosis in hyperuricemic rats.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37446016</pmid><doi>10.3390/ijms241310839</doi><orcidid>https://orcid.org/0000-0002-0371-0361</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adefovir dipivoxil Angiotensin II Animals c-Kit protein Cell activation Creatinine Diet Fibrosis Gelatinase A Health aspects Histopathology Hyperglycemia Hyperlipidemia Hypertension Hyperuricemia Hyperuricemia - metabolism Kidney - metabolism Kidney diseases Kidney Diseases - metabolism Mast cells Mast Cells - metabolism Oxidation Oxidative Stress Rats Risk factors Signal Transduction Smad2 protein Sodium cromoglycate Transforming Growth Factor beta1 - metabolism Transforming growth factor-b1 Transforming growth factors Uric acid Valsartan |
| title | Accumulation of Renal Fibrosis in Hyperuricemia Rats Is Attributed to the Recruitment of Mast Cells, Activation of the TGF-β1/Smad2/3 Pathway, and Aggravation of Oxidative Stress |
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