» Articles » PMID: 38158445

Muscone Inhibits Angiotensin II-induced Cardiac Hypertrophy Through the STAT3, MAPK and TGF-β/SMAD Signaling Pathways

Overview
Journal Mol Biol Rep
Specialty Molecular Biology
Date 2023 Dec 29
PMID 38158445
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Muscone is a chemical monomer derived from musk. Although many studies have confirmed the cardioprotective effects of muscone, the effects of muscone on cardiac hypertrophy and its potential mechanisms are unclear.The aim of the present study was to investigate the effect of muscone on angiotensin (Ang) II-induced cardiac hypertrophy.

Methods And Results: In the present study, we found for the first time that muscone exerted inhibitory effects on Ang II-induced cardiac hypertrophy and cardiac injury in mice. Cardiac function was analyzed by echocardiography measurement, and the degree of cardiac fibrosis was determined by the quantitative real-time polymerase chain reaction (qRT-PCR), Masson trichrome staining and western blot assay. Secondly, qRT-PCR experiment showed that muscone attenuated cardiac injury by reducing the secretion of pro-inflammatory cytokines and promoting the secretion of anti-inflammatory cytokines. Moreover, western blot analysis found that muscone exerted cardio-protective effects by inhibiting phosphorylation of key proteins in the STAT3, MAPK and TGF-β/SMAD pathways. In addition, CCK-8 and determination of serum biochemical indexes showed that no significant toxicity or side effects of muscone on normal cells and organs.

Conclusions: Muscone could attenuate Ang II-induced cardiac hypertrophy, in part, by inhibiting the STAT3, MAPK, and TGF-β/SMAD signaling pathways.

Citing Articles

The protective role of muscone in the development of COPD.

Feng T, Guo X, Chen W, Zhang Y, Dai R, Zhang Y Front Immunol. 2025; 16:1508879.

PMID: 40034710 PMC: 11872711. DOI: 10.3389/fimmu.2025.1508879.


Targeting the mTOR Pathway in Hepatocellular Carcinoma: The Therapeutic Potential of Natural Products.

Chen G, Zhang Y, Zhou Y, Luo H, Guan H, An B J Inflamm Res. 2024; 17:10421-10440.

PMID: 39659752 PMC: 11630751. DOI: 10.2147/JIR.S501270.

References
1.
Jiang J, Lan C, Li L, Yang D, Xia X, Liao Q . A novel porcupine inhibitor blocks WNT pathways and attenuates cardiac hypertrophy. Biochim Biophys Acta Mol Basis Dis. 2018; 1864(10):3459-3467. DOI: 10.1016/j.bbadis.2018.07.035. View

2.
Gu J, Qiu M, Lu Y, Ji Y, Qian Z, Sun W . Piperlongumine attenuates angiotensin-II-induced cardiac hypertrophy and fibrosis by inhibiting Akt-FoxO1 signalling. Phytomedicine. 2021; 82:153461. DOI: 10.1016/j.phymed.2021.153461. View

3.
Chen D, Li Z, Bao P, Chen M, Zhang M, Yan F . Nrf2 deficiency aggravates Angiotensin II-induced cardiac injury by increasing hypertrophy and enhancing IL-6/STAT3-dependent inflammation. Biochim Biophys Acta Mol Basis Dis. 2019; 1865(6):1253-1264. DOI: 10.1016/j.bbadis.2019.01.020. View

4.
Cheng Y, Shen A, Wu X, Shen Z, Chen X, Li J . Qingda granule attenuates angiotensin II-induced cardiac hypertrophy and apoptosis and modulates the PI3K/AKT pathway. Biomed Pharmacother. 2020; 133:111022. DOI: 10.1016/j.biopha.2020.111022. View

5.
Oldfield C, Duhamel T, Dhalla N . Mechanisms for the transition from physiological to pathological cardiac hypertrophy. Can J Physiol Pharmacol. 2019; 98(2):74-84. DOI: 10.1139/cjpp-2019-0566. View