ArticlePharmaceutical biology2022
Sericin-mediated improvement of dysmorphic cardiac mitochondria from hypercholesterolaemia is associated with maintaining mitochondrial dynamics, energy production, and mitochondrial structure.
Article in Pharmaceutical biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Post-translational acylation of proteins in cardiac hypertrophy.Nature reviews. Cardiology · 2025Review
- Sericin Protein: Structure, Properties, and Applications.Journal of functional biomaterials · 2024Review
- Silkworm Cocoon: Dual Functions as a Traditional Chinese Medicine and the Raw Material of Promising Biocompatible Carriers.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Article
- Review
- Article
- Modified Linggui Zhugan Decoction protects against ventricular remodeling through ameliorating mitochondrial damage in post-myocardial infarction rats.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextSericin is a component protein in the silkworm cocoon [
objectiveTo investigate the mechanism of action of sericin in cardiac mitochondria under hypercholesterolaemia. MATERIALS AND
methodsHypercholesterolaemia was induced in Wistar rats by feeding them 6% cholesterol-containing chow for 6 weeks. The hypercholesterolemic rats were separated into 2 groups (
resultsA 32.22 ± 2.9% increase in the percent striated area of cardiac muscle was observed in sericin-treated hypercholesterolemic rats compared to the nontreatment group (4.18 ± 1.11%). Alterations in mitochondrial proteins, including upregulation of optic atrophy 1 (OPA1) and reduction of NADH-ubiquinone oxidoreductase 75 kDa subunit (NDUFS1) expression, are correlated with a reduction in mitochondrial apoptosis under sericin treatment. Differential proteomic observation also revealed that sericin may improve mitochondrial energy production by upregulating acetyl-CoA acetyltransferase (ACAT1) and NADH dehydrogenase 1α subcomplex subunit 10 (NDUFA10) expression. DISCUSSION AND
conclusionsSericin treatment could improve the dysmorphic mitochondrial structure, metabolism, and energy production of cardiac mitochondria under hypercholesterolaemia. These results suggest that sericin may be an alternative treatment molecule that is related to cardiac mitochondrial abnormalities.
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