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February 6, 2026European Heart Journal

Sting reestablishes mitochondrial homeostasis in heart failure

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Key result

STING activation preserves mitochondrial homeostasis and improves cardiac function in pressure-overload heart failure.

Why the study?

Does STING activation improve cardiac function and mitochondrial homeostasis in a mouse model of pressure overload-induced heart failure?

Population

Mice subjected to transvers aortic constriction surgery, including cardiomyocyte-specific STING conditional…

Comparison

STING activation via pharmacological agonist or… vs TAC-only controls, or STING inhibition via…

Design

Preclinical

Follow-up

2 weeks

Authors

THTuolisi HeryedUniversity of Tokyo HospitalMKM KatohUniversity of Tokyo HospitalSNS NomuraUniversity of Tokyo Hospital

Discussion

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Implication

STING signaling exerts a cardioprotective effect during pressure overload by maintaining mitochondrial homeostasis and energy balance in cardiomyocytes.

Key Points

  • The study aims to clarify the role of STING signaling in cardiomyocytes during heart failure.
  • Subjected mice to transvers aortic constriction surgery to model heart failure.
  • Administered STING pharmacological modulators (C176 inhibitor and DMXAA agonist).
  • Generated CM-specific STING knockout and overexpression models.
  • Conducted single-cell RNA sequencing and proteomic analysis on isolated cardiomyocytes.
  • C176-treated mice exhibited worsened cardiac function, while DMXAA treatment preserved it.
  • STING knockout mice showed exacerbated cardiac dysfunction after pressure overload.
  • Overexpression of STING in cardiomyocytes partially rescued cardiac function.
  • Activation of STING restored mitochondrial dynamics and maintained homeostasis.

Structured PICO

Does STING activation improve cardiac function and mitochondrial homeostasis in a mouse model of pressure overload-induced heart failure?

P
Population
Mice subjected to transvers aortic constriction (TAC) surgery, including cardiomyocyte-specific STING conditional knockout (cK.O.) mice and cardiomyocyte-specific STING overexpression (OE) mice.
I
Intervention
STING activation via pharmacological agonist (DMXAA) or cardiomyocyte-specific STING overexpression (OE).
C
Comparator
TAC-only controls, or STING inhibition via pharmacological inhibitor (C176) or cardiomyocyte-specific STING conditional knockout (cK.O.).
O
Outcome
Cardiac function and mitochondrial homeostasis (fission and mitophagy).surrogate

STING signaling exerts a cardioprotective effect during pressure overload by maintaining mitochondrial homeostasis and energy balance in cardiomyocytes.

Cite This Study

Heryed et al. (2025) studied Heart failure. STING activation (DMXAA or genetic overexpression) vs. TAC-only controls or STING inhibition/knockout was evaluated on Cardiac function and mitochondrial homeostasis. STING activation in cardiomyocytes preserved mitochondrial fission and mitophagy, maintained mitochondrial homeostasis, and improved cardiac function in mice subjected to pressure overload.

synapsesocial.com/papers/698585678f7c464f23008a9fhttps://doi.org/10.1093/eurheartj/ehaf784.4724
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