Biomolecules in Myocarditis and Inflammatory Heart Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 75

Special Issue Editor


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Guest Editor
Department of Clinical Sciences and Pharmacy, High Point University, High Point, NC, USA
Interests: intermediate metabolite signaling; intracardiac cell–cell cross-talk between cardiomyocytes and non-cardiomyocytes; metabolomic signaling; spatial metabolomics; metabolite–protein interactions; post-translational modifications by intermediate metabolites; endoplasmic reticulum stress; oxidative stress; nitrosative stress
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Special Issue Information

Dear Colleagues,

The aim of this Special Issue of Biomolecules is to explore the genetic and immunological aspects underlying myocarditis, pericarditis, and inflammatory heart disease. These multifactorial diseases have diverse etiologies, including autoimmune mechanisms, drug-induced hypersensitivity reactions, and viral and non-viral infections, among others. Irrespective of the cause, the pathophysiology is characterized by an inflammatory cascade that leads to myocyte injury, adverse ventricular remodeling, interstitial fibrosis, and functional impairment. Unfortunately, a significant subset of patients progress to dilated cardiomyopathy (DCM), chronic heart failure, and high-mortality cardiac-related conditions. Investigations into immunological responses and how genetics may influence inflammatory pathways can provide the basis for new therapeutic options.

Dr. Amarylis Claudine Bonito A. Wanschel
Guest Editor

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Keywords

  • cardiomyocyte
  • macrophage
  • cardiac remodeling
  • oxidative and nitrosative stress
  • neutrophils

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Published Papers (1 paper)

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Research

19 pages, 5378 KiB  
Article
Dual Regulation of Mitochondrial Complexes by H2S via S-Sulfhydration Controls Respiration in Type 1 Diabetic Hearts
by Tong Su, Li Han Zhu, Jun Xian Liu, Li Yuan Jin, Huixing Cui, Longhao Yu and Yin Hua Zhang
Biomolecules 2025, 15(8), 1197; https://doi.org/10.3390/biom15081197 - 20 Aug 2025
Abstract
Hydrogen sulfide (H2S) has been established to regulate mitochondrial respiration and ATP production, but whether the regulation is through S-sulfhydration (-SSH) of mitochondrial complexes is not well understood. Recently, H2S is known to exert diverse and dose-dependent effects [...] Read more.
Hydrogen sulfide (H2S) has been established to regulate mitochondrial respiration and ATP production, but whether the regulation is through S-sulfhydration (-SSH) of mitochondrial complexes is not well understood. Recently, H2S is known to exert diverse and dose-dependent effects on mitochondrial complexes. However, the involvement of S-sulfhydration of each mitochondrial complex and the activities in diabetic hearts have not been revealed. Here, we conducted comprehensive investigations into S-sulfhydration and the activities of mitochondrial complexes I–V in normal and Streptozotocin (STZ)-induced type 1 diabetic (DM) heart mitochondria. Results showed that proteins of H2S-producing enzymes were downregulated in DM heart mitochondria, which was accompanied by reduced mitochondrial membrane potential (MMP), greater ROS, and lower complex I and V activities, reduced complex V-SSH in DM. In both groups, supplementation with the H2S donor NaHS increased the S-sulfhydration of all mitochondrial complexes, and the activities of complexes I–III and V were significantly increased but complex IV activity was reduced. Consequently, mitochondrial MMP, ROS, and ATP production were normalized with NaHS in DM, whereas inhibition of H2S generation increased mitochondrial ROS and reduced MMP via reducing complex activities in both groups. Ischemic reperfusion did not affect NaHS-increment of S-sulfhydration of complexes I–V, but significantly impaired complex V activity in DM. Collectively, H2S-dependent S-sulfhydration of mitochondrial complexes I–V in normal and DM heart mitochondria were involved in the activation of mitochondrial complexes I–III/V and the inhibition of complex IV, which control cardiac mitochondrial respiration and ATP production. Full article
(This article belongs to the Special Issue Biomolecules in Myocarditis and Inflammatory Heart Disease)
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