Sacubitril/valsartan combination enhanced cardiac glycophagy and prevented the progression of murine diabetic cardiomyopathy

Elshenawy, Dina Salem Abdelaziz; Ramadan, Nehal M.; Abdo, Vivian Boshra; Ashour, Rehab H.

doi:10.1016/j.biopha.2022.113382

Cited by 4 publications

(1 citation statement)

References 73 publications

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“…This study first demonstrated that glycogen pathology in DCM is associated with glycophagy induction. New study shows that sacubitril/valsartan combination alleviates DCM in mice by enhancing STBD1‐mediated glycophagy (Elshenawy et al, 2022). Interestingly, women with diabetes are at higher risk of heart failure than men, the mechanisms of sex‐dependent metabolic stress‐related cardiac pathology have not been elucidated.…”

Section: Stbd1 and Nonneoplastic Diseasesmentioning

confidence: 99%

Glycogen‐binding protein STBD1: Molecule and role in pathophysiology

Tang

Liu

Zhao

et al. 2023

Journal Cellular Physiology

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Starch‐binding domain‐containing protein 1 (STBD1) is a glycogen‐binding protein discovered in skeletal muscle gene differential expression that is pivotal to cellular energy metabolism. Recent studies have indicated that STBD1 is involved in many physiological processes, such as glycophagy, glycogen accumulation, and lipid droplet formation. Moreover, dysregulation of STBD1 causes multiple diseases, including cardiovascular disease, metabolic disease, and even cancer. Deletions and/or mutations in STBD1 promote tumorigenesis. Therefore, STBD1 has garnered considerable interest in the pathology community. In this review, we first summarized the current understanding of STBD1, including its structure, subcellular localization, tissue distribution, and biological functions. Next, we examined the roles and molecular mechanisms of STBD1 in related diseases. Based on available research, we discussed the novel function and future of STBD1, including its potential application as a therapeutic target in glycogen‐related diseases. Given the significance of STBD1 in energy metabolism, an in‐depth understanding of the protein is crucial for understanding physiological processes and developing therapeutic strategies for related diseases.

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Section: Stbd1 and Nonneoplastic Diseasesmentioning

confidence: 99%

Glycogen‐binding protein STBD1: Molecule and role in pathophysiology

Tang

Liu

Zhao

et al. 2023

Journal Cellular Physiology

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Jellyfish stings‐induced cardiac failure was ameliorated through AAG‐mediated glycogen‐driven ATP production

Qin,

Chen,

Liu

et al. 2024

Exploration

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Jellyfish stings have become a common injury among fishermen and divers. Severe jellyfish stings could worsen cardiac function and even cause cardiac complications, ultimately leading to cardiac failure (CF). Currently, there are no effective drugs available. Single cell sequencing revealed alpha‐1 acid glycoprotein (AAG), an energy regulatory protein targeting to glycogen, was highly expressed in jellyfish stings‐induced CF patients. However, the mechanism remains elusive. It is postulated that AAG could increase glycogen metabolism, protecting against jellyfish stings‐induced CF. AAG deletion exacerbated CF, while exogenous and endogenous AAG ameliorated CF. AAG also rescued the decline triggered by the AAG knockout (KO). Intriguingly, AAG improved cardiac function and metabolic adaptation by glycogen‐driven ATP production, shifting mitochondrial/glycolytic ATP production towards glycolysis. Sorted by single‐cell RNA sequencing and spatial transcription technology, CC‐chemokine receptor 5 (CCR5) and Peroxisome proliferator‐activated receptor‐gamma coactivator‐1alpha (PGC‐1α) were differentially expressed. Mechanistically, CCR5 inhibitor MVC abolished AAG's protective effect and PGC‐1α overexpression. Collectively, jellyfish stings‐induced CF was ameliorated through AAG‐mediated glycogen‐driven ATP production, promoting glycolytic/mitochondrial metabolic switches to rely energetically primarily on glycolysis, which might serve as a therapeutic target of CF.

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