What does this research mean for the field?

Hydrogen sulfide alleviates diabetic cardiomyopathy by inhibiting inflammatory and fibrotic responses mediated by the JAK2/STAT3 signaling pathway. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

The aim is to elucidate how hydrogen sulfide alleviates diabetic cardiomyopathy through pathway inhibition.

June 11, 2026International ImmunopharmacologyOpen Access

Network pharmacology and experimental validation reveal inhibition of the JAK2/STAT3 pathway by hydrogen sulfide in diabetic cardiomyopathy

Q: What is the clinical evidence from this study?

Study design: Other. Population: Diabetic cardiomyopathy. Intervention: Hydrogen sulfide (H2S) donor sodium hydrosulfide (NaHS). Primary outcome: Myocardial fibrosis, inflammation, and cardiac function.

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Key result

Hydrogen sulfide improves cardiac function and reduces myocardial fibrosis in db/db mice via JAK2/STAT3 inhibition.

Why the study?

Although hydrogen sulfide has known cardioprotective properties in diabetic cardiomyopathy, its underlying molecular mechanisms remain incompletely defined.

Population

db/db mice with DCM and high-glucose stimulated cardiac fibroblasts

Comparison

H2S donor sodium hydrosulfide vs control

Design

Preclinical network pharmacology and experimental validation study

Follow-up

8 weeks

Authors

PYPing Yang TLTe Li TLTingting Liu

Discussion

Member takes

Overview

Should not change clinical practice in diabetic cardiomyopathy; hypothesis-generating for hydrogen sulfide donors in preclinical models.

Key Points

The aim is to elucidate how hydrogen sulfide alleviates diabetic cardiomyopathy through pathway inhibition.
Developed a type 2 diabetes-associated diabetic cardiomyopathy model using db/db mice.
Administered sodium hydrosulfide (NaHS) for 8 weeks and analyzed cardiac function through functional, histological, and molecular evaluations.
Conducted network pharmacology analyses to identify and validate potential therapeutic targets.
NaHS treatment significantly reduced myocardial fibrosis and inflammation in db/db mice.
Improvement in cardiac function was noted alongside a marked inhibition of JAK2/STAT3 pathway activation.
Pharmacological reactivation of STAT3 reversed the protective effects of hydrogen sulfide both in vivo and in vitro.

Structured PICO

Population

db/db mice with spontaneous type 2 diabetes-associated diabetic cardiomyopathy treated for 8 weeks.

Intervention

H2S donor sodium hydrosulfide (NaHS) for 8 weeks

Comparator

Untreated diabetic models (implied)

Outcome

Cardiac function, myocardial fibrosis, and inflammationsurrogate

Hydrogen sulfide protects against diabetic cardiomyopathy by inhibiting the JAK2/STAT3 signaling pathway, reducing inflammation and fibrosis.

Cite This Study

Yang et al. (2026) studied Diabetic cardiomyopathy. Hydrogen sulfide (H2S) donor sodium hydrosulfide (NaHS) was evaluated on Myocardial fibrosis, inflammation, and cardiac function. Hydrogen sulfide treatment significantly attenuated myocardial fibrosis and inflammation in db/db mice, improving cardiac function by inhibiting the JAK2/STAT3 signaling pathway.

synapsesocial.com/papers/6a2a4ff180c8f91e7f39ca0d https://doi.org/10.1016/j.intimp.2026.116959

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June 11, 2026International ImmunopharmacologyOpen Access

Network pharmacology and experimental validation reveal inhibition of the JAK2/STAT3 pathway by hydrogen sulfide in diabetic cardiomyopathy

View Full Paper

Ask AI

Bookmark

Key result

Hydrogen sulfide improves cardiac function and reduces myocardial fibrosis in db/db mice via JAK2/STAT3 inhibition.

Why the study?

Although hydrogen sulfide has known cardioprotective properties in diabetic cardiomyopathy, its underlying molecular mechanisms remain incompletely defined.

Population

db/db mice with DCM and high-glucose stimulated cardiac fibroblasts

Comparison

H2S donor sodium hydrosulfide vs control

Design

Preclinical network pharmacology and experimental validation study

Follow-up

8 weeks

Authors

PYPing Yang TLTe Li TLTingting Liu

Discussion

Member takes

Overview

Should not change clinical practice in diabetic cardiomyopathy; hypothesis-generating for hydrogen sulfide donors in preclinical models.

Key Points

The aim is to elucidate how hydrogen sulfide alleviates diabetic cardiomyopathy through pathway inhibition.
Developed a type 2 diabetes-associated diabetic cardiomyopathy model using db/db mice.
Administered sodium hydrosulfide (NaHS) for 8 weeks and analyzed cardiac function through functional, histological, and molecular evaluations.
Conducted network pharmacology analyses to identify and validate potential therapeutic targets.
NaHS treatment significantly reduced myocardial fibrosis and inflammation in db/db mice.
Improvement in cardiac function was noted alongside a marked inhibition of JAK2/STAT3 pathway activation.
Pharmacological reactivation of STAT3 reversed the protective effects of hydrogen sulfide both in vivo and in vitro.

Structured PICO

Population

db/db mice with spontaneous type 2 diabetes-associated diabetic cardiomyopathy treated for 8 weeks.

Intervention

H2S donor sodium hydrosulfide (NaHS) for 8 weeks

Comparator

Untreated diabetic models (implied)

Outcome

Cardiac function, myocardial fibrosis, and inflammationsurrogate

Hydrogen sulfide protects against diabetic cardiomyopathy by inhibiting the JAK2/STAT3 signaling pathway, reducing inflammation and fibrosis.

Cite This Study

synapsesocial.com/papers/6a2a4ff180c8f91e7f39ca0d https://doi.org/10.1016/j.intimp.2026.116959

Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

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