ReviewJournal of pharmaceutical analysis2024
Potential of natural drug modulation of endoplasmic reticulum stress in the treatment of myocardial injury.
Review in Journal of pharmaceutical analysis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The trial behind it
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Who cites it
22 citing papers in PubMed.
- Graveoumarins A-C: chiral resolution, absolute configuration, and anticoagulant/anti-inflammatory activities of 3'-methyl-3'-butenyl coumarins fromPharmaceutical biology · 2026Article
- Therapeutic Timing at Mitochondrial Redox-Autophagy-Mitophagy Checkpoints in Age-Related Hearing Loss.Molecular neurobiology · 2026Review
- Nine anthropometric insulin resistance indices predict mortality and life expectancy across glucose states.iScience · 2026Article
- Ginsenoside Rb1 inhibits oxidative stress and ferroptosis to alleviate salpingitis infertility by down-regulating PTGS2 and up-regulating GPX4.Journal of ginseng research · 2026Article
- TMEM87a Maintains Cardiomyocyte Integrity by Limiting Ferroptosis in Dilated Cardiomyopathy.Annals of the New York Academy of Sciences · 2026Article
- ACOT1-specific expression modulates metabolic reprogramming in diabetic cardiomyopathy: The role of SREBP1c lactylation in CD36-mediated lipotoxicity.American heart journal plus : cardiology research and practice · 2026Article
- Metformin improves cardiac stress tolerance and mitochondrial function during early aging.Experimental gerontology · 2026Article
- The potential of TRPC channel-mediated autophagy in myocardial ischemia-reperfusion injury.Journal of cardiothoracic surgery · 2026Review
- UCMSC-derived exosomal circDLGAP4 enhances HFF-1 cell proliferation and migration by promoting ZNF217 promoter H3K27 acetylation.Molecular genetics and genomics : MGG · 2026Article
- The Integrated Stress Response Protein, eIF2α, Modulates UPRCardiovascular toxicology · 2026Article
- In vivo dynamic nuclear polarization magnetic resonance imaging reveals cardiac mitochondrial redox imbalance as an early indicator of heart failure.Redox biology · 2026Article
- Ion channels and GPCRs as pharmacological regulators of ferroptosis and pyroptosis in metabolic diseases.Diabetology & metabolic syndrome · 2026Review
- Cardioprotective Role of CalhexCell biochemistry and biophysics · 2026Review
- Angelica sinensis polysaccharide nanoparticles can improve myocardial ischemia-reperfusion injury by inhibiting ferritinophagy via the ATF6/NCOA4 pathway.Journal of translational medicine · 2026Article
- Mechanosensitive Ion Channels: Molecular Hubs Integrating Skeletal Muscle Adaptation and Systemic Homeostasis.International journal of biological sciences · 2026Review
- Role of recombinant S100A13 expression in regulating mitochondrial fission and fusion in lung epithelial cells.BBA advances · 2026Article
- Cross-tissue single-cell atlas reveals Id2 promotes sepsis-induced tissue damage by mediating macrophage metabolic reprogramming via Pkm2.International journal of biological sciences · 2026Article
- Mitochondria-enriched nanovesicles: A novel approach for treating radiation-induced skin injury.Materials today. Bio · 2025Article
- Review
- Ligustrazine nano-drug delivery system ameliorates doxorubicin-mediated myocardial injury via piezo-type mechanosensitive ion channel component 1-prohibitin 2-mediated mitochondrial quality surveillance.Journal of nanobiotechnology · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial injury (MI) is a common occurrence in clinical practice caused by various factors such as ischemia, hypoxia, infection, metabolic abnormalities, and inflammation. Such damages are characterized by a reduction in myocardial function and cardiomyocyte death that can result in dangerous outcomes such as cardiac failure and arrhythmias. An endoplasmic reticulum stress (ERS)-induced unfolded protein response (UPR) is triggered by several stressors, and its intricate signaling networks are instrumental in both cell survival and death. Cardiac damage frequently triggers ERS in response to different types of injuries and stress. High levels of ERS can exacerbate myocardial damage by inducing necrosis and apoptosis. To target ERS in MI prevention and treatment, current medical research is focused on identifying effective therapy approaches. Traditional Chinese medicine (TCM) is frequently used because of its vast range of applications and low risk of adverse effects. Various studies have demonstrated that active components of Chinese medicines, including polyphenols, saponins, and alkaloids, can reduce myocardial cell death, inflammation, and modify the ERS pathway, thus preventing and mitigating cardiac injury. Thus, this paper aims to provide a new direction and scientific basis for targeting ERS in MI prevention and treatment. We specifically summarize recent research progress on the regulation mechanism of ERS in MI by active ingredients of TCM.
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