What question did this study set out to answer?

This research aims to assess the role of C/EBPβ in regulating myocardial fibrosis and remodeling via the ACE2/Ang-(1-7) pathway in hypertensive heart disease.

April 12, 2026Journal of Cellular and Molecular MedicineOpen Access

Targeting C/ EBP β to Suppress Myocardial Fibrosis in Hypertensive Heart Disease: Role of the ACE2 /Ang‐(1–7) Pathway

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Key result

C/EBPβ overexpression in hypertensive rats lowers BP, improves cardiac function, and reduces fibrosis via ACE2.

Why the study?

Hypertensive heart disease features ventricular remodelling and fibrosis driven by RAS dysregulation, but whether C/EBPβ attenuates this through the ACE2/Ang-(1-7) axis was unknown.

Does C/EBPβ overexpression attenuate myocardial fibrosis and remodeling in a rat model of hypertensive heart disease?

Comparison

Lentiviral C/EBPβ vs C/EBPβ shRNA vs negative control vs saline

Design

Preclinical animal and in vitro laboratory study

Authors

YTYuanyuan TieSecond Affiliated Hospital of Xi'an Jiaotong University ZLZehao LinSun Yat-sen University MZMing ZhangSecond Affiliated Hospital of Xi'an Jiaotong University

Discussion

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Implication

Should not yet change practice in hypertensive heart disease; extends preclinical evidence for C/EBPβ as therapeutic target.

Key Points

This research aims to assess the role of C/EBPβ in regulating myocardial fibrosis and remodeling via the ACE2/Ang-(1-7) pathway in hypertensive heart disease.
Used spontaneously hypertensive rats for in vivo investigation.
Administered lentiviral vectors for C/EBPβ overexpression or knockdown.
Evaluated cardiac function through echocardiography and histological analysis.
Measured serum and myocardial levels of angiotensin II and Ang-(1-7).
Studied primary rat cardiac fibroblasts under Ang II stimulation.
C/EBPβ overexpression reduced arterial pressure and improved cardiac function.
Demonstrated a reduction in myocardial fibrosis and collagen deposition.
Shifting of the renin-angiotensin system toward the ACE2/Ang-(1-7) axis was observed.
C/EBPβ activation correlated with increased ACE2 and decreased inflammatory markers.
Knockdown of C/EBPβ did not significantly affect cardiac outcomes.

Structured PICO

Does C/EBPβ overexpression attenuate myocardial fibrosis and remodeling in a rat model of hypertensive heart disease?

Population

Eight-week-old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (n=24 total, 6 per group), as well as primary rat cardiac fibroblasts.

Intervention

Tail-vein injection of lentiviral vectors encoding C/EBPβ or C/EBPβ short hairpin RNA (shRNA). In vitro: lentiviral C/EBPβ overexpression combined with ACE2-specific or control siRNA.

Comparator

Lentiviral negative control in SHR, and saline injection in normotensive Wistar-Kyoto rats.

Outcome

Blood pressure, echocardiographic parameters, cardiac hypertrophy, and myocardial fibrosis at 12 weeks after injection.surrogate

C/EBPβ overexpression attenuates hypertensive cardiac remodeling and fibrosis by shifting the renin-angiotensin system towards the protective ACE2/Ang-(1-7) pathway.

Cite This Study

Tie et al. (2026) studied this question. C/EBPβ overexpression in hypertensive rats lowered blood pressure, improved cardiac function, and attenuated myocardial fibrosis via the ACE2/Ang-(1-7) axis.

synapsesocial.com/papers/69db380f4fe01fead37c6311 https://doi.org/10.1111/jcmm.71139

Topics

Molecular Mechanisms of Cardiac Remodeling Hypertension management

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Targeting C/ EBP β to Suppress Myocardial Fibrosis in Hypertensive Heart Disease: Role of the ACE2 /Ang‐(1–7) Pathway

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Targeting C/ EBP β to Suppress Myocardial Fibrosis in Hypertensive Heart Disease: Role of the ACE2 /Ang‐(1–7) Pathway

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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