The role and clinical significance of the miR‑378a‑3p/MAPK1 axis in hypertensive vascular remodeling

BACKGROUND: Primary hypertension is a prevalent cardiovascular disease contributing to a heavy global health burden. To investigate serum miR‑378a‑3p expression in hypertensive patients and its mechanism in OX‑LDL‑mediated vascular smooth muscle cell (VSMC) dysfunction. METHOD: 286 primary hypertension patients and 132 healthy controls were enrolled, and serum miR‑378a‑3p levels and clinical parameters were detected. ROC curve and multivariate logistic regression were applied for diagnostic and risk factor analyses. In vitro cultured human aortic VSMCs were used to assess cell function, and phenotypic transformation via qRT‑PCR, CCK‑8, Transwell, and Western blot. Target gene binding was verified by bioinformatics and dual‑luciferase assay. RESULTS: miR‑378a‑3p was significantly reduced in hypertension sufferers, and served as an independent protective factor, whereas LDL‑C, PRA, Ang II, and ALD were independent risk factors. OX‑LDL downregulated miR‑378a‑3p and promoted VSMC dysfunction, while miR‑378a‑3p overexpression alleviated these injuries by directly targeting MAPK1. CONCLUSION: miR-378a-3p shows potential as an auxiliary screening biomarker for hypertension risk stratification and may serve as a promising therapeutic target by regulating VSMC function via MAPK1.

Authors

Institutions

Publication Details

Journal
American Journal of Hypertension
Published
2026-07-30
DOI
https://doi.org/10.1093/ajh/hpag096
Primary Topic
MicroRNA in disease regulation
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

The role and clinical significance of the miR‑378a‑3p/MAPK1 axis in hypertensive vascular remodeling

Shuping Wang, Li Liu, Shirong Hu, Li Li
American Journal of Hypertension
MicroRNA in disease regulation
article

The role and clinical significance of the miR‑378a‑3p/MAPK1 axis in hypertensive vascular remodeling

Shuping Wang, Li Liu, Shirong Hu, Li Li
article en

Abstract

BACKGROUND: Primary hypertension is a prevalent cardiovascular disease contributing to a heavy global health burden. To investigate serum miR‑378a‑3p expression in hypertensive patients and its mechanism in OX‑LDL‑mediated vascular smooth muscle cell (VSMC) dysfunction. METHOD: 286 primary hypertension patients and 132 healthy controls were enrolled, and serum miR‑378a‑3p levels and clinical parameters were detected. ROC curve and multivariate logistic regression were applied for diagnostic and risk factor analyses. In vitro cultured human aortic VSMCs were used to assess cell function, and phenotypic transformation via qRT‑PCR, CCK‑8, Transwell, and Western blot. Target gene binding was verified by bioinformatics and dual‑luciferase assay. RESULTS: miR‑378a‑3p was significantly reduced in hypertension sufferers, and served as an independent protective factor, whereas LDL‑C, PRA, Ang II, and ALD were independent risk factors. OX‑LDL downregulated miR‑378a‑3p and promoted VSMC dysfunction, while miR‑378a‑3p overexpression alleviated these injuries by directly targeting MAPK1. CONCLUSION: miR-378a-3p shows potential as an auxiliary screening biomarker for hypertension risk stratification and may serve as a promising therapeutic target by regulating VSMC function via MAPK1.

American Journal of Hypertension
Beijing University of Chinese Medicine (CN), Panzhihua University (CN), Panzhihua Central Hospital (CN)
Good health and well-being
Openalex Percentile: Top 12%
MicroRNA in disease regulation
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.