ArticleJournal of translational medicine2018
Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum stress apoptosis signaling pathway in ischemia reperfusion-induced acute kidney injury.
Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 62 citations in OpenAlex.
- O-Glycosylation of E-Cadherin Induced by Endoplasmic Reticulum Stress Negatively Regulates Cell Polarity and Proliferation in Acute Kidney Injury.Journal of biochemical and molecular toxicology · 2026Article
- Brazilin attenuates kidney ischemia-reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction.Histology and histopathology · 2026Article
- Integrated transcriptomics identifies ER stress-associated apoptosis in post-resuscitation AKI and supports early Dl-3-n-butylphthalide-associated renoprotection in a porcine TCA model.Frontiers in pharmacology · 2026Article
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- Early Administration of N-Acetylcysteine Provides Renal and Cardiac Mitochondrial and Redox Protection, Preventing the Development of Cardio-Renal Syndrome Type IV Induced by 5/6NX.Antioxidants (Basel, Switzerland) · 2025Article
- Cellular senescence in renal ischemia-reperfusion injury.Chinese medical journal · 2025Review
- Butyrolactone-I from Marine Fungal Metabolites Mitigates Heat-Stress-Induced Apoptosis in IPEC-J2 Cells and Mice Through the ROS/PERK/CHOP Signaling Pathway.Marine drugs · 2024Article
- New Therapeutic Method for Alleviating Damage of Acute Kidney Injury ThroughInternational journal of molecular sciences · 2024Article
- Effect of Sodium Thiosulfate Pre-Treatment on Renal Ischemia-Reperfusion Injury in Kidney Transplantation.International journal of molecular sciences · 2024Article
- Connexin32 gap junction channels deliver miR155-3p to mediate pyroptosis in renal ischemia-reperfusion injury.Cell communication and signaling : CCS · 2024Article
- Acute kidney injury: exploring endoplasmic reticulum stress-mediated cell death.Frontiers in pharmacology · 2024Review
- Data driven analysis reveals prognostic genes and immunological targets in human sepsis-associated acute kidney injury.World journal of emergency medicine · 2024Article
- 4-Octyl itaconate alleviates renal ischemia reperfusion injury by ameliorating endoplasmic reticulum stress via Nrf2 pathway.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- RNA sequencing and bioinformatics analysis of circular RNAs in asphyxial newborns with acute kidney injury.The Kaohsiung journal of medical sciences · 2023Article
- Functioning and mechanisms of PTMs in renal diseases.Frontiers in pharmacology · 2023Review
- Cellular senescence in ischemia/reperfusion injury.Cell death discovery · 2022Review
- Demethylation of H3K9 and H3K27 Contributes to the Tubular Renal Damage Triggered by Endoplasmic Reticulum Stress.Antioxidants (Basel, Switzerland) · 2022Article
- Hydrogen sulfide plays a potential alternative for the treatment of metabolic disorders of diabetic cardiomyopathy.Molecular and cellular biochemistry · 2022Review
- Verbena Attenuates Adriamycin-Induced Renal Tubular Injury via Inhibition of ROS-ERK1/2-NLRP3 Signal Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Fucoxanthin Attenuates Oxidative Damage by Activating the Sirt1/Nrf2/HO-1 Signaling Pathway to Protect the Kidney from Ischemia-Reperfusion Injury.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIschemia-reperfusion (I/R)-induced acute kidney injury (AKI) not only prolongs the length of hospital stay, but also seriously affects the patient's survival rate. Although our previous investigation has verified that reactive oxygen species (ROS) transferred through gap junction composed of connexin32 (Cx32) contributed to AKI, its underlying mechanisms were not fully understood and viable preventive or therapeutic regimens were still lacking. Among various mechanisms involved in organs I/R-induced injuries, endoplasmic reticulum stress (ERS)-related apoptosis is currently considered to be an important participant. Thus, in present study, we focused on the underlying mechanisms of I/R-induced AKI, and postulated that Cx32 mediated ROS/ERS/apoptosis signal pathway activation played an important part in I/R-induced AKI.
methodsWe established renal I/R models with Cx32
resultsRenal damage was progressively exacerbated in a time-dependent manner at the reperfusion stage, that was consistent with the alternation of ERS activation, including glucose regulated protein 78 (BiP/GRP78), X box-binding protein1, and C/EBP homologous protein expression. TUDCA or 4-PBA application attenuated I/R-induced ERS activation and protected against renal tubular epithelial cells apoptosis and renal damage. Cx32 deficiency decreased ROS generation and distribution between the neighboring cells, which attenuated I/R-induced ERS activation, and improved cell apoptosis and renal damage.
conclusionCx32 mediated ROS/ERS/apoptosis signal pathway activation played an important part in I/R-induced AKI. Cx32 deficiency, ROS elimination, and ERS inhibition all could protect against I/R-induced AKI.
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