The association between microRNA-21 and hypertension-induced cardiac remodeling

Area of Science:

• Cardiovascular Biology
• Molecular Medicine
• Hypertension Research

Background:

• Hypertension causes cardiac remodeling, including hypertrophy and fibrosis, leading to hypertensive heart disease (HHD).
• The role of microRNA-21 (miR-21) in hypertension-induced cardiac remodeling is not well understood.
• Elevated circulating miR-21 levels and correlation with fibrotic markers suggest its involvement in HHD.

Purpose of the Study:

• To investigate the role of miR-21 in cardiac remodeling associated with hypertension.
• To elucidate the molecular mechanisms by which miR-21 influences cardiac fibrosis and hypertrophy.
• To determine if inhibiting miR-21 can prevent or reverse hypertension-induced cardiac changes.

Main Methods:

• Assessed circulating miR-21 levels in HHD patients and control subjects.
• Measured miR-21 expression in mouse hearts subjected to angiotensin II infusion or transverse aortic constriction (TAC).
• Investigated the expression of miR-21 targets (PDCD4, AP-1, TGF-β1) in vivo and in vitro using neonatal rat cardiomyocytes.

Main Results:

• Circulating miR-21 was higher in HHD patients and correlated with fibrotic markers.
• MiR-21 expression was upregulated in mouse hearts after Ang II infusion or TAC.
• PDCD4 expression decreased, while AP-1 and TGF-β1 increased in response to hypertension stimuli.
• Inhibition of miR-21 in cardiomyocytes attenuated Ang II-induced PDCD4 downregulation and AP-1/TGF-β1 signaling.

Conclusions:

• MiR-21 plays a significant role in hypertension-induced cardiac remodeling.
• The miR-21/PDCD4/AP-1/TGF-β1 pathway is a key mechanism in cardiac fibrosis and hypertrophy.
• Targeting miR-21 offers a potential therapeutic strategy for preventing or treating hypertensive heart disease.