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Long Noncoding RNA MALAT1: Salt-Sensitive Hypertension.

Mohd Mabood Khan1, Annet Kirabo1

  • 1Department of Medicine, Preston Research Building, Vanderbilt University Medical Centre, Nashville, TN 37232, USA.

International Journal of Molecular Sciences
|May 25, 2024
PubMed
Summary
This summary is machine-generated.

High salt intake causes hypertension by increasing oxidative stress via epithelial sodium channels. Long noncoding RNA MALAT1 exacerbates this by upregulating Keap1, inhibiting the antioxidant Nrf2 pathway. Inhibiting MALAT1 may treat hypertension.

Keywords:
MALAT1hypertensioninflammationlong noncoding RNAsalt

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Area of Science:

  • Cardiovascular Science
  • Molecular Biology
  • Immunology

Background:

  • Hypertension is a leading cause of global mortality, linked to cardiovascular disease.
  • Elevated salt intake promotes inflammation and hypertension via antigen-presenting cells (APCs).
  • Oxidative stress, lipid peroxidation, and isolevuglandin formation are key inflammatory mediators.

Purpose of the Study:

  • To explore the role of long noncoding RNA MALAT1 in the Keap1-Nrf2-antioxidant defense pathway in salt-induced hypertension.
  • To investigate MALAT1's potential as a therapeutic target for hypertension and cardiovascular disease.

Main Methods:

  • Investigated the epithelial sodium channel (ENaC) role in sodium-induced APC activation and oxidative stress.
  • Examined the regulation of MALAT1 expression by sodium and its impact on Keap1 and Nrf2.
  • Assessed the effect of MALAT1 silencing on sodium-induced Keap1 upregulation and Nrf2 nuclear translocation.

Main Results:

  • Sodium intake activates APCs through ENaC, increasing oxidative stress and inflammation.
  • MALAT1 expression is upregulated by sodium via Sp1, leading to increased Keap1 and inhibited Nrf2.
  • Silencing MALAT1 reverses sodium-induced Keap1 upregulation, promoting Nrf2 activity and antioxidant gene expression.

Conclusions:

  • MALAT1, through the Keap1-Nrf2 pathway, modulates antioxidant defense in hypertension.
  • MALAT1 inhibition offers a potential therapeutic strategy for salt-induced hypertension and cardiovascular disease.