Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Aug;479(8):1895-1908.
doi: 10.1007/s11010-023-04816-x. Epub 2023 Aug 1.

Possible role of LCZ696 in atherosclerosis: new inroads and perspective

Hayder M Al-Kuraishy  1 , Ali I Al-Gareeb  1 , Engy Elekhnawy  2 , Gaber El-Saber Batiha  3
Affiliations
Review

Possible role of LCZ696 in atherosclerosis: new inroads and perspective

Hayder M Al-Kuraishy et al. Mol Cell Biochem. 2024 Aug.

Abstract

LCZ696 blocks both angiotensin receptor type 1 (ATR1) and neprilysin (NEP), which are intricate in the degradation of natriuretic peptides (NPs) and other endogenous peptides. It has been shown NEP inhibitors and LCZ696 could be effectively in the management of atherosclerosis (AS). However, the underlying mechanism of LCZ696 in AS is needed to be clarified entirely. Hence, this review is directed to reconnoiter the mechanistic role of LCZ696 in AS. The anti-inflammatory role of LCZ696 is related to the inhibition of transforming growth factor beta (TGF-β)-activated kinase 1 (TAK) and nod-like receptor pyrin 3 receptor (NLRP3) inflammasome. Moreover, LCZ696, via inhibition of pro-inflammatory cytokines, oxidative stress, apoptosis and endothelial dysfunction can attenuate the development and progression of AS. In conclusion, LCZ696 could be effective in the management of AS through modulation of inflammatory and oxidative signaling. Preclinical and clinical studies are recommended in this regard.

Keywords: Atherosclerosis; Cytokines; LCZ696; Pro-inflammatory.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

References

    1. Nalivaeva NN, Zhuravin IA, Turner AJ (2020) Neprilysin expression and functions in development, ageing and disease. Mech Ageing Dev 1(192):111363
    1. Wang Y, Zhou R, Lu C, Chen Q, Xu T, Li D (2019) Effects of the angiotensin-receptor neprilysin inhibitor on cardiac reverse remodeling: meta-analysis. J Am Heart Assoc 8(13):e012272 - PubMed
    1. Solomon SD, McMurray JJ, Anand IS, Ge J, Lam CS, Maggioni AP, Martinez F, Packer M, Pfeffer MA, Pieske B, Redfield MM (2019) Angiotensin–neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med 381(17):1609–1620 - PubMed
    1. Pardossi-Piquard R, Dunys J, Yu G, StGeorge-Hyslop P, Alves da Costa C, Checler F (2006) Neprilysin activity and expression are controlled by nicastrin. J Neurochem 97(4):1052–6 - PubMed
    1. Bayes-Genis A, Prickett TC, Richards AM, Barallat J, Lupón J (2016) Soluble neprilysin retains catalytic activity in heart failure. J Heart Lung Transplant 35(5):684–685 - PubMed

MeSH terms

LinkOut - more resources