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 Oct 28:2024:1821252.
doi: 10.1155/2024/1821252. eCollection 2024.

Targeting lncRNA MALAT1: A Promising Approach to Overcome Metabolic Syndrome

Affiliations
Review

Targeting lncRNA MALAT1: A Promising Approach to Overcome Metabolic Syndrome

Gulandanmu Aihemaiti et al. Int J Endocrinol. .

Abstract

Metabolic syndrome (MetS) is a collection of metabolic abnormalities including insulin resistance, atherogenic dyslipidemia, central obesity, and hypertension. Recently, long noncoding RNAs (lncRNAs) have emerged as pivotal regulators of metabolic balance, influencing the genes associated with MetS. Although the prevalence of insulin resistance is rising, leading to an increased risk of type 2 diabetes mellitus (T2DM) and its vascular complications, there is still a notable gap in understanding the role of lncRNAs in the context of clinical diabetes. Among lncRNAs, lung adenocarcinoma metastasis-associated transcript 1 (MALAT1) has been identified as a significant regulator of metabolism-related disorders, including T2DM and cardiovascular disease (CVD). This review explores the mechanism of lncRNA MALAT1 and suggests that targeting it could offer a promising strategy to combat MetS, thereby enhancing the prognosis of MetS.

Keywords: LncRNA MALAT1; dyslipidemia; dysregulated glucose homeostasis; hypertension; insulin resistance; metabolic syndrome.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Characteristics of MetS and the relationship between lncRNA MALAT1.
Figure 2
Figure 2
Relevant role of lncRNA MALAT1 in metabolic syndrome.
Figure 3
Figure 3
MALAT1 and related classic signaling pathways.

References

    1. Fahed G., Aoun L., Bou Zerdan M., et al. Metabolic Syndrome: Updates on Pathophysiology and Management in 2021. International Journal of Molecular Sciences . 2022;23(2):p. 786. doi: 10.3390/ijms23020786. - DOI - PMC - PubMed
    1. Agus A., Clément K., Sokol H. Gut Microbiota-Derived Metabolites as Central Regulators in Metabolic Disorders. Gut . 2021;70(6):1174–1182. doi: 10.1136/gutjnl-2020-323071. - DOI - PMC - PubMed
    1. Reaven G. M. Role of Insulin Resistance in Human Disease (Syndrome X): an Expanded Definition. Annual Review of Medicine . 1993;44(1):121–131. doi: 10.1146/annurev.me.44.020193.001005. - DOI - PubMed
    1. McCracken E., Monaghan M., Sreenivasan S. Pathophysiology of the Metabolic Syndrome. Clinics in Dermatology . 2018;36(1):14–20. doi: 10.1016/j.clindermatol.2017.09.004. - DOI - PubMed
    1. Hoffman E. L., VonWald T., Hansen K. The Metabolic Syndrome. South Dakota Medicine: The Journal of the South Dakota State Medical Association . 2015:24–28. - PubMed

LinkOut - more resources