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Title:
Canagliflozin improves high-salt-induced aortic arteriosclerosis and premature aging in dahl salt-sensitive rats through the SIRT6/HIF-1 α signaling pathway | Molecular and Cellular Biochemistry
Description:
Hypertension and its complications seriously affect human health, bringing about long-term medical burdens, functional impairments and even death. This study explored the impact of Canagliflozin (CANA) on the blood vessels of salt-sensitive hypertension. Male Dahl salt-sensitive (Dahl SS) rats were fed with an 8% high-salt diet, and then intragastrically given CANA at a dose of 30 mg/kg/day or with a 0.5% hydroxypropyl methylcellulose solution for 12 weeks to induce hypertensive vascular damage and premature aging. Through vascular ultrasound detection, CANA improved the aortic stiffness and hemodynamics of high-salt-fed rats. Through vascular reactivity tests, CANA improved the carotid artery vasodilation. Hematoxylin and eosin (H&E), Sirius red, and senescence associated β-galactosidase staining were performed on the aorta, and CANA improved the fibrosis and aging of the aorta. CANA was found to reduce the expression of senescence associated secretory phenotype in the circulation that was induced by a high-salt diet. Additionally, it increased the expression of Sirtuin 6(SIRT6) in blood vessels and decreased the expression of Hypoxia-inducible factor 1α (HIF-1α) and its target genes. This study has demonstrated for the first time that CANA mitigates salt-induced aortic sclerosis and premature aging via the SIRT6/HIF-1α pathway.
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Keywords {š}
pubmed, article, google, scholar, cas, central, aging, wang, zhang, data, hypertension, vascular, hebei, sirt, cell, curation, signaling, pathway, res, heart, httpsdoiorgs, rats, senescence, endothelial, canagliflozin, aortic, expression, sci, shijiazhuang, china, premature, cana, int, cells, mol, department, peoples, republic, hospital, software, dahl, guo, blood, sirtuin, access, liu, kidney, disease, general, privacy,
Topics {āļø}
mir-126a-3p targets hif-1alpha p53/mirnas/ccna2 pathway serves wnt/β-catenin signaling induces regulating sirt6/hif-1alpha axis hypoxia-induced pulmonary hypertension modulating hypoxia-induced chemokine canonical p53/p21 pathway sirt6/hif-1α pathway age-treated endothelial cells month download article/chapter d-galactose-induced liver hif-1alpha/pdk4 signaling pi3k/akt signaling pathways p53/p21-independent manner high-salt-fed rats hypoxia-inducible factor-1alpha hypoxia-inducible factor 1α sodium-glucose cotransporter-2 inhibitors dahl salt-sensitive rats sirt6/ho-1 signaling long-term medical burdens heart salt-specific overexpression male dahl salt-sensitive vascular endothelial cells p53/p21 pathway 8% high-salt diet high-salt diet cellular biochemistry aims sirt6 promotes angiogenesis endothelial senescence contributes ampk-dependent pathway metalloproteinase-9tissue inhibitor high-salt intake sodium-glucose cotransporter 2 salt-sensitive hypertension regulating hif-1α abdominal aortic aneurysm full article pdf premature vascular aging sirt6 regulates autophagy hypoxic pulmonary hypertension high sodium intake p53/p21/p16 large arterial stiffness mesenchymal stem cells hypertensive heart failure physical examination center sirt1āpten signaling privacy choices/manage cookies hif-1α transgene
Questions {ā}
- Adam CA, Anghel R, Marcu DTM et al (2022) Impact of sodium-glucose cotransporter 2 (SGLT2) inhibitors on arterial stiffness and vascular aging-What do we know so far?
- Scisciola L, Olivieri F, Ambrosino C et al (2023) On the wake of metformin: do anti-diabetic SGLT2 inhibitors exert anti-aging effects?
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headline:Canagliflozin improves high-salt-induced aortic arteriosclerosis and premature aging in dahl salt-sensitive rats through the SIRT6/HIF-1 α signaling pathway
description:Hypertension and its complications seriously affect human health, bringing about long-term medical burdens, functional impairments and even death. This study explored the impact of Canagliflozin (CANA) on the blood vessels of salt-sensitive hypertension. Male Dahl salt-sensitive (Dahl SS) rats were fed with an 8% high-salt diet, and then intragastrically given CANA at a dose of 30 mg/kg/day or with a 0.5% hydroxypropyl methylcellulose solution for 12 weeks to induce hypertensive vascular damage and premature aging. Through vascular ultrasound detection, CANA improved the aortic stiffness and hemodynamics of high-salt-fed rats. Through vascular reactivity tests, CANA improved the carotid artery vasodilation. Hematoxylin and eosin (H&E), Sirius red, and senescence associated β-galactosidase staining were performed on the aorta, and CANA improved the fibrosis and aging of the aorta. CANA was found to reduce the expression of senescence associated secretory phenotype in the circulation that was induced by a high-salt diet. Additionally, it increased the expression of Sirtuin 6(SIRT6) in blood vessels and decreased the expression of Hypoxia-inducible factor 1α (HIF-1α) and its target genes. This study has demonstrated for the first time that CANA mitigates salt-induced aortic sclerosis and premature aging via the SIRT6/HIF-1α pathway.
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headline:Canagliflozin improves high-salt-induced aortic arteriosclerosis and premature aging in dahl salt-sensitive rats through the SIRT6/HIF-1 α signaling pathway
description:Hypertension and its complications seriously affect human health, bringing about long-term medical burdens, functional impairments and even death. This study explored the impact of Canagliflozin (CANA) on the blood vessels of salt-sensitive hypertension. Male Dahl salt-sensitive (Dahl SS) rats were fed with an 8% high-salt diet, and then intragastrically given CANA at a dose of 30 mg/kg/day or with a 0.5% hydroxypropyl methylcellulose solution for 12 weeks to induce hypertensive vascular damage and premature aging. Through vascular ultrasound detection, CANA improved the aortic stiffness and hemodynamics of high-salt-fed rats. Through vascular reactivity tests, CANA improved the carotid artery vasodilation. Hematoxylin and eosin (H&E), Sirius red, and senescence associated β-galactosidase staining were performed on the aorta, and CANA improved the fibrosis and aging of the aorta. CANA was found to reduce the expression of senescence associated secretory phenotype in the circulation that was induced by a high-salt diet. Additionally, it increased the expression of Sirtuin 6(SIRT6) in blood vessels and decreased the expression of Hypoxia-inducible factor 1α (HIF-1α) and its target genes. This study has demonstrated for the first time that CANA mitigates salt-induced aortic sclerosis and premature aging via the SIRT6/HIF-1α pathway.
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name:Department of Geriatric Cardiology, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
type:PostalAddress
type:Organization
email:[email protected]
PostalAddress:
name:Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Peopleās Republic of China
name:Department of Geriatric Cardiology, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Peopleās Republic of China
name:Department of Geriatric Cardiology, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Geriatric Cardiology, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Geriatric Cardiology, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Geriatric Cardiology, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Physical Examination Center, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Cardiology, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Cardiology, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Internal Medicine, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Peopleās Republic of China
name:Department of Cardiology, The Third Hospital of Shijiazhuang City Affiliated to Hebei Medical University, Shijiazhuang, Peopleās Republic of China
name:Department of Physiology, Hebei Medical University, Hebei, China
name:Hebei Key Laboratory of Metabolic Diseases, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Geriatric Cardiology, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
name:Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Peopleās Republic of China
name:Department of Geriatric Cardiology, Hebei General Hospital, Shijiazhuang, Peopleās Republic of China
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