SNF472: mechanism of action and results from clinical trials

Sinha, Smeeta; Raggi, Paolo; Chertow, Glenn M.

doi:10.1097/mnh.0000000000000726

Cited by 9 publications

(5 citation statements)

References 35 publications

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“…24 The pathophysiological alteration caused by the arterial stiffening in media sclerosis assists to systolic hypertension and congestive heart failure. 25 The incidence and prognosis of cardiovascular events should be significantly improved via preventing or rescuing pathogenesis of VC.…”

Section: Discussionmentioning

confidence: 99%

Ameliorative effect of allicin on vascular calcification via inhibiting endoplasmic reticulum stress

Wang

Lin

et al. 2021

Vascular

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Objectives Vascular calcification (VC) is an independent predictor for cardiovascular events and mortality. However, there are currently no effective methods to reverse or prevent it. The present study aimed to determine the ameliorative effect of allicin on VC. Methods VC model of rats was induced by high-dose vitamin D3, which was valued by Alizarin Red staining, calcium contents, and alkaline phosphatase in the aorta. Systolic blood pressure, pulse pressure, and pulse wave velocity were measured to determine aortic stiffness. Protein levels were detected by Western blot. Results Allicin treatment rescued aortic VC and stiffness. The increased protein levels of RUNX2 and BMP2, two markers of osteoblastic phenotype of vascular smooth muscle cells, in the calcified aorta were attenuated by allicin, whereas the decreased levels of calponin and SM22α induced by calcification were improved. Allicin treatment significantly attenuated the increased protein levels of GRP78, GRP94, and CHOP, which are key markers of endoplasmic reticulum stress, in the calcified aorta. The activation of PERK/eIF2α/ATF4 cascades was also prevented by allicin. Conclusions Allicin could ameliorate aortic VC and stiffness. The ameliorative effect of allicin on VC might be mediated by inhibiting PERK/eIF2α/ATF4 cascades. Our results might provide a new proof for VC treatment.

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Section: Discussionmentioning

confidence: 99%

Ameliorative effect of allicin on vascular calcification via inhibiting endoplasmic reticulum stress

Wang

Lin

et al. 2021

Vascular

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“…Phytate is a potential nutrient for VC treatment 297 . SNF472, which acts as an exogenous source of phytate, exerts an inhibitory effect on VC 298–300 . The clinical trial proved that an adequate prescription of phytate can protect against AAC in CKD patients 301 .…”

Section: Potential Therapeutic Strategies Of Vcmentioning

confidence: 96%

“… 297 SNF472, which acts as an exogenous source of phytate, exerts an inhibitory effect on VC. 298 , 299 , 300 The clinical trial proved that an adequate prescription of phytate can protect against AAC in CKD patients. 301 Inositol hexakisphosphate (IP6, phytic acid), an endogenous compound existing widespread in mammalian cells or tissues, inhibits the mineralization of osteoblast cultures to protect against VC.…”

Section: Potential Therapeutic Strategies Of Vcmentioning

confidence: 99%

Vascular calcification: Molecular mechanisms and therapeutic interventions

Pan

Jie

Huang

2023

MedComm

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Vascular calcification (VC) is recognized as a pathological vascular disorder associated with various diseases, such as atherosclerosis, hypertension, aortic valve stenosis, coronary artery disease, diabetes mellitus, as well as chronic kidney disease. Therefore, it is a life‐threatening state for human health. There were several studies targeting mechanisms of VC that revealed the importance of vascular smooth muscle cells transdifferentiating, phosphorous and calcium milieu, as well as matrix vesicles on the progress of VC. However, the underlying molecular mechanisms of VC need to be elucidated. Though there is no acknowledged effective therapeutic strategy to reverse or cure VC clinically, recent evidence has proved that VC is not a passive irreversible comorbidity but an active process regulated by many factors. Some available approaches targeting the underlying molecular mechanism provide promising prospects for the therapy of VC. This review aims to summarize the novel findings on molecular mechanisms and therapeutic interventions of VC, including the role of inflammatory responses, endoplasmic reticulum stress, mitochondrial dysfunction, iron homeostasis, metabolic imbalance, and some related signaling pathways on VC progression. We also conclude some recent studies on controversial interventions in the clinical practice of VC, such as calcium channel blockers, renin–angiotensin system inhibitions, statins, bisphosphonates, denosumab, vitamins, and ion conditioning agents.

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“…Currently, numerous methods exist to decrease vascular calcification in dialysis patients, such as the utilization of vitamin K1 [ 66 ], subcutaneous insulin and heparin [ 67 ], as well as the use of sodium thiosulfate [ 68 ], bisphosphonate [ 69 ], and inositol hexaphosphate hexasodium salt (SNF) 472 [ 70 ]. These drugs have been tested for treating vascular calcification in dialysis patients and have proven to be effective.…”

Section: Risk Factor Management Of Hf In Dialysis Patientsmentioning

confidence: 99%

Management of Chronic Heart Failure in Dialysis Patients: A Challenging but Rewarding Path

Guo,

Ji,

Sun

et al. 2024

Rev. Cardiovasc. Med.

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Chronic heart failure (CHF) is a common complication and cause of death in dialysis patients. Although several clinical guidelines and expert consensus on heart failure (HF) in the general population have been issued in China and abroad, due to abnormal renal function or even no residual renal function (RRF) in dialysis patients, the high number of chronic complications, as well as the specificity, variability, and limitations of hemodialysis (HD) and peritoneal dialysis (PD) treatments, there are significant differences between dialysis patients and the general population in terms of the treatment and management of HF. The current studies are not relevant to all dialysis-combined HF populations, and there is an urgent need for high-quality studies on managing HF in dialysis patients to guide and standardize treatment. After reviewing the existing guidelines and literature, we focused on the staging and diagnosis of HF, management of risk factors, pharmacotherapy, and dialysis treatment in patients on dialysis. Based on evidence-based medicine and clinical trial data, this report reflects new perspectives and future trends in the diagnosis and treatment of HF in dialysis patients, which will further enhance the clinicians’ understanding of HF in dialysis patients.

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SNF472: mechanism of action and results from clinical trials

Cited by 9 publications

References 35 publications

Ameliorative effect of allicin on vascular calcification via inhibiting endoplasmic reticulum stress

Ameliorative effect of allicin on vascular calcification via inhibiting endoplasmic reticulum stress

Vascular calcification: Molecular mechanisms and therapeutic interventions

Management of Chronic Heart Failure in Dialysis Patients: A Challenging but Rewarding Path

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