ArticleFrontiers in pharmacology2020
Sacubitril/Valsartan Reduces Fibrosis and Alleviates High-Salt Diet-Induced HFpEF in Rats.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Sacubitril/Valsartan Improves Functional Capacity and Reverses LV Remodeling in Obese Patients with Hypertrophic HFpEF: A Randomized Open-Label Study.Journal of clinical medicine · 2026Article
- Sacubitril/valsartan as a modulator of pulmonary fibrosis: insights into Lnc-SNHG-16/miR-455 modulation and Notch/Smad-3 pathway inhibition.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The Combined Empagliflozin and Sacubitril/Valsartan Therapy Attenuates Isoproterenol-Induced Heart Failure in Rats: Functional, Molecular, and Structural Insights.Cardiovascular drugs and therapy · 2026Article
- Article
- Sacubitril/valsartan mitigates cisplatin-induced liver injury through modulation of oxidative stress, Caspase-3 activity, and RXR-α signaling in experimental rats.Frontiers in pharmacology · 2026Article
- Predicting cardiac and renal responses to sacubitril/valsartan with a mathematical model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2025Article
- Risk factors for major cardiovascular adverse events and the effects of sacubitril/valsartan in patients with acute myocardial infarction after Percutaneous Coronary Intervention.Pakistan journal of medical sciences · 2025Article
- LCZ696, an angiotensin receptor-neprilysin inhibitor, ameliorates epithelial-mesenchymal transition of peritoneal mesothelial cells and M2 macrophage polarization.Renal failure · 2024Article
- Co-Delivery of Valsartan and Metformin from a Thermosensitive Hydrogel-Nanoparticle System Promotes Collagen Production in Proliferating and Senescent Primary Human Dermal Fibroblasts.Biomacromolecules · 2024Article
- Sacubitril/Valsartan Alleviates Cardiac Remodeling and Dysfunction in L-NAME-Induced Hypertension and Hypertensive Heart Disease.Biomedicines · 2024Article
- Fibroblasts and immune cells: at the crossroad of organ inflammation and fibrosis.American journal of physiology. Heart and circulatory physiology · 2024Review
- Signaling Pathways and Potential Therapeutic Strategies in Cardiac Fibrosis.International journal of molecular sciences · 2023Review
- Reviewing the Modern Therapeutical Options and the Outcomes of Sacubitril/Valsartan in Heart Failure.International journal of molecular sciences · 2022Review
- Article
- Sacubitril/valsartan in Heart Failure and Beyond-From Molecular Mechanisms to Clinical Relevance.Reviews in cardiovascular medicine · 2022Review
- Angiotensin receptor-neprilysin inhibitors for hypertension-hemodynamic effects and relevance to hypertensive heart disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Review
- Molecular mechanisms of sacubitril/valsartan in cardiac remodeling.Frontiers in pharmacology · 2022Review
- Protective Effects of Sacubitril/Valsartan on Cardiac Fibrosis and Function in Rats With Experimental Myocardial Infarction Involves Inhibition of Collagen Synthesis by Myocardial Fibroblasts Through Downregulating TGF-β1/Smads Pathway.Frontiers in pharmacology · 2021Article
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14 authors.
Funding
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Abstract
Previous studies have confirmed the clinical efficacy of sacubitril/valsartan (Sac/Val) for the treatment of heart failure with reduced ejection fraction (HFrEF). However, the role of Sac/Val in heart failure with preserved ejection fraction (HFpEF) remains unclear. Sac/Val is a combination therapeutic medicine comprising sacubitril and valsartan that acts as a first angiotensin receptor blocker and neprilysin inhibitor (angiotensin-receptor neprilysin inhibitor (ARNI)). Here, we investigated the role of Sac/Val in high-salt diet-induced HFpEF coupled with vascular injury as well as the underlying mechanism. Rats were fed with high-salt feed, followed by intragastric administration of Sac/Val (68 mg/kg; i.g.). The results of functional tests revealed that a high-salt diet caused pathological injuries in the heart and vascular endothelium, which were significantly reversed by treatment with Sac/Val. Moreover, Sac/Val significantly decreased the levels of fibrotic factors, including type I collagen and type Ⅲ collagen, thus, reducing the ratio of MMP2/TIMP2 while increasing Smad7 levels. Further investigation suggested that Sac/Val probably reversed the effects of high-salt diet-induced HFpEF by inhibiting the activation of the TGF-β1/Smad3 signaling pathway. Thus, treatment with Sac/Val effectively alleviated the symptoms of high-salt diet-induced HFpEF, probably by inhibiting fibrosis via the TGF-β1/Smad3 signaling pathway, supporting the therapeutic potential of Sac/Val for the treatment of HFpEF.
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