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Effective drugs for the treatment of myocardial fibrosis (MF) are lacking. Traditional Chinese medicine (TCM) has garnered increasing attention in recent years for the prevention and treatment of myocardial fibrosis. This Article describes the pathogenesis of myocardial fibrosis from the modern medicine, along with the research progress. Reports suggest that Chinese medicine may play a role in ameliorating myocardial fibrosis through different regulatory mechanisms such as reduction of inflammatory reaction and oxidative stress, inhibition of cardiac fibroblast activation, reduction in extracellular matrix, renin-angiotensin-aldosterone system regulation, transforming growth Factor-β1 (TGF-β1) expression downregulation, TGF-β1/Smad signalling pathway regulation, and microRNA expression regulation. Therefore, traditional Chinese medicine serves as a valuable source of candidate drugs for exploration of the mechanism of occurrence and development, along with clinical prevention and treatment of MF.

Background In patients with established HF, low triiodothyronine syndrome (LT3S) is commonly present, and N-terminal pro-B-type natriuretic peptide (NT-proBNP) is a useful marker for predicting death. This study was aimed to evaluate the prognostic value of LT3S in combination with NT-proBNP for risk of death in patients with heart failure (HF). Methods A total of 594 euthyroid patients hospitalized with acute decompensated HF were enrolled by design. Of these patients, 27 patients died during hospitalization and 100 deaths were identified in patients discharged alive during one year follow-up. Patients were divided into 2 groups on the base of the reference ranges of free T3 (FT3) levels: LT3S group (FT3 < 2.3pg/mL, n = 168) and non-LT3S group (FT3 ≥ 2.3pg/mL, n = 426). Results In multivariable Cox regression, LT3S was significantly associated with 1 year all-cause mortality (adjusted hazard ratio, 1.85; 95 % confidence interval [CI], 1.21 to 2.82; P = 0.005), but not significant for in-hospital mortality (adjusted hazard ratio, 1.58; 95 % CI, 1.58 to 2.82; P = 0.290) after adjustment for clinical variables and NT-proBNP. Addition of LT3S and NT-proBNP to the prediction model with clinical variables significantly improved the C statistic for predicting 1 year all-cause mortality. Conclusions In patients with acute decompensated HF, the combination of LT3S and NT-proBNP improved prediction for 1 year all-cause mortality beyond established risk factors, but was not strong enough for in-hospital mortality.

The present study aimed to reveal the bioactive compounds and molecular mechanisms of Qishen Yixin Granules (QSYXG) in the treatment of MF using an integrated network pharmacology and pharmacological validation approach. All active ingredients, drug targets, MF genes were screened from the TCMSP database, drug-target databases, GeneCard database, respectively. Functional and pathway enrichment analyses were operated through the clusterProfiler package in R programming language. Experimental validation was performed using haematoxylin-eosin staining, Masson’s trichrome staining and immunohistochemistry in isoproterenol-induced MF rats, and western blot analysis, phalloidin staining and immunofluorescence staining were used to elucidate the predicted mechanism on H9C2 cells. In this study, 55 bioactive components and 59 putative targets were collected. Functional enrichment analysis revealed that responses to lipopolysaccharides, oxidative stress and hypoxia were the key biological processes and were regulated simultaneously by six direct targets, including PTGS2, MAPK14, AKT1, MAPK8, IL-6 and IL-1β. Five pathways were determined by KEGG pathway enrichment analysis. The experiment results indicate QSYXG could down-regulated expression of PTGS2, MAPK14 and MAPK8 and up-regulated expression of AKT1 in the treatment of MF. This study revealed QSYXG could alleviate MF based on multiple components, targets and pathways.