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作者

Ang Liu, Bin Su

作者单位

Affiliations ¹ Department of Anesthesiology, Heze Hospital Affiliated of Shandong First Medical University, Heze Municipal Hospital, Heze, Shandong, China. ² Department of Anesthesiology, Heze Hospital Affiliated of Shandong First Medical University, Heze Municipal Hospital, Heze, Shandong, China. Electronic address: doctorsue@12 com.

刊名

International immunopharmacology

年份

2026

卷号

Vol.188

页码

117297

ISSN

1878-1705

关键词

Cardiac fibroblasts Diabetic cardiomyopathy Hydrogen sulfide JAK2/STAT3 signaling Myocardial fibrosis Network pharmacology.

摘要

Yang et al. investigated the protective effects of hydrogen sulfide against diabetic cardiomyopathy and proposed inhibition of JAK2/STAT3 signaling as a central mechanism. Their integration of network pharmacology with in vivo and in vitro experiments provides valuable evidence linking sodium hydrosulfide treatment to reduced myocardial inflammation and fibrosis. However, several issues may limit the causal interpretation of these findings. First, STAT3 prioritization was based on a small transc...更多

Yang et al. investigated the protective effects of hydrogen sulfide against diabetic cardiomyopathy and proposed inhibition of JAK2/STAT3 signaling as a central mechanism. Their integration of network pharmacology with in vivo and in vitro experiments provides valuable evidence linking sodium hydrosulfide treatment to reduced myocardial inflammation and fibrosis. However, several issues may limit the causal interpretation of these findings. First, STAT3 prioritization was based on a small transcriptomic dataset, nominal significance thresholds, and an exceptionally broad list of hydrogen sulfide-related targets. Second, the pharmacological rescue experiment lacked Colivelin-alone and clearly matched vehicle-control groups, making it difficult to distinguish pathway-specific reversal from the independent effects of Colivelin. Third, the high-glucose fibroblast experiments did not include an osmotic control. Finally, hydrogen sulfide bioavailability, endogenous hydrogen sulfide-producing enzymes, and systemic metabolic parameters were not assessed. Addressing these limitations through more rigorous bioinformatic thresholds, complete pharmacological controls, genetic validation, osmotic controls, and direct exposure measurements would strengthen the proposed mechanistic link between hydrogen sulfide, JAK2/STAT3 inhibition, and protection against diabetic cardiomyopathy.收起

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