ArticleMolecular medicine reports2016
Sequential changes of endoplasmic reticulum stress and apoptosis in myocardial fibrosis of diabetes mellitus-induced rats.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Gene expression, MMGBSA, molecular and induced-fit docking of Bambusa vulgaris phytocompounds in endoplasmic reticulum stress induced by streptozotocin.Molecular biology reports · 2026Article
- Cellular and Molecular Pathways in Diabetes-Associated Heart Failure: Emerging Mechanistic Insights and Therapeutic Opportunities.Current issues in molecular biology · 2025Review
- Sea buckthorn flavonoids and their derivatives: potential natural compounds for the treatment of diabetic cardiomyopathy.Frontiers in pharmacology · 2025Review
- Importance of unfolded protein response modulation on diabetes management: a systematic review.Journal of diabetes and metabolic disorders · 2024Review
- Subacute cadmium exposure modulates Th1 polarization to trigger ER stress-induced porcine hepatocyte apoptosis via regulation of miR-369-TNFα axis.Environmental science and pollution research international · 2022Article
- Cryptotanshinone alleviates myocardial ischemia and reperfusion injury in rats to mitigate ER stress-dependent apoptosis by modulating the JAK1/STAT3 axis.American journal of translational research · 2022Article
- Molecular and cellular mechanisms in diabetic heart failure: Potential therapeutic targets.Frontiers in endocrinology · 2022Review
- Protective Effects of L-Theanine on IPEC-J2 Cells Growth Inhibition Induced by Dextran Sulfate Sodium via p53 Signaling Pathway.Molecules (Basel, Switzerland) · 2021Article
- Advanced Glycation End Products: New Clinical and Molecular Perspectives.International journal of environmental research and public health · 2021Review
- Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside.Frontiers in cardiovascular medicine · 2020Review
- Astragaloside IV ameliorates endoplasmic reticulum stress‑induced apoptosis of Aβ25‑35‑treated PC12 cells by inhibiting the p38 MAPK signaling pathway.Molecular medicine reports · 2019Article
- Dexmedetomidine Attenuates Myocardial Ischemia-Reperfusion Injury in Diabetes Mellitus by Inhibiting Endoplasmic Reticulum Stress.Journal of diabetes research · 2019Article
- Of mice and men: models and mechanisms of diabetic cardiomyopathy.Basic research in cardiology · 2018Review
- Hypothermia and Rewarming Activate a Macroglial Unfolded Protein Response Independent of Hypoxic-Ischemic Brain Injury in Neonatal Piglets.Developmental neuroscience · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endoplasmic reticulum (ER) is an organelle in which proteins form their appropriate structures. However, several of these proteins become unfolded or misfolded when exposed to stimuli, including hyperglycemia, oxidative stress, ischemia, disturbance of calcium homeostasis and overexpression of abnormal proteins, which activates ER stress and the unfolded protein response (UPR). To date, investigations have demonstrated that ER stress is important in diabetic myocardial fibrosis by inducing cardiac cell apoptosis. Therefore, in the present study, the polymerase chain reaction, western blotting analysis and tissue staining were performed to identify the changes in UPR signaling proteins and apoptotic proteins in diabetic rats at different time points, and to determine whether the myocardial fibrosis is associated with ER-stress-mediated apoptosis using a diabetes mellitus (DM) rat model. It was found that the upregulation of ER stress markers and apoptotic molecules developed over time. It was also demonstrated that anti‑apoptotic markers and proapoptotic markers were activated early following model establishment, and then decreased in months 4 and 5. The changes in myocardial fibrosis were found to accelerate in a time-dependent manner with apoptosis in the DM rats.
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Registered trials
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