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 lowered blood pressure, improved cardiac function, and attenuated myocardial fibrosis via the ACE2/Ang-(1-7) axis.

Why the study?

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 and normotensive Wistar-Kyoto rats, as well as primary…

Comparison

Tail-vein injection of lentiviral vectors… vs Lentiviral negative control in SHR, and saline…

Design

Preclinical

Follow-up

12 weeks

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

Member takes

Implication

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

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

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Implication

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