ArticleCardiovascular drugs and therapy2022
Protective Role of lncRNA TTN-AS1 in Sepsis-Induced Myocardial Injury Via miR-29a/E2F2 Axis.
Article in Cardiovascular drugs and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- Genomic structural equation modeling reveals shared genetic structure of cardiac function and structure-function association studies of CLCNKA mutations.Scientific reports · 2026Article
- Sepsis-induced cardiac dysfunction: mitochondria and energy metabolism.Intensive care medicine experimental · 2025Review
- The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025Review
- Construction of a competitive endogenous RNA network and identification of potential regulatory axes in hypertrophic cardiomyopathy.Frontiers in cardiovascular medicine · 2025Article
- Article
- LncRNA DLEU1 contributes to the progression of septic myocardial dysfunction by targeting miR-381-3p.Central-European journal of immunology · 2024Article
- ELF5-Regulated lncRNA-TTN-AS1 Alleviates Myocardial Cell Injury via Recruiting PCBP2 to Increase CDK6 Stability in Myocardial Infarction.Molecular and cellular biology · 2024Article
- Revealing Landscape of Competing Endogenous RNA Networks in Sepsis-Induced Cardiovascular Diseases.Reviews in cardiovascular medicine · 2023Review
- Network pharmacology-based approach to explore the underlying mechanism of sinomenine on sepsis-induced myocardial injury in rats.Frontiers in pharmacology · 2023Article
- Identification and Validation of Immune-Related Biomarker Gene and Construction of ceRNA Networks in Septic Cardiomyopathy.Frontiers in cellular and infection microbiology · 2022Article
- Research Progress on the Mechanism of Sepsis Induced Myocardial Injury.Journal of inflammation research · 2022Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveApproximately 50% of patients with sepsis encounter myocardial injury. The mortality of septic patients with cardiac dysfunction (approx. 70%) is much higher than that of patients with sepsis only (20%). A large number of studies have suggested that lncRNA TTN-AS1 promotes cell proliferation in a variety of diseases. This study delves into the function and mechanism of TTN-AS1 in sepsis-induced myocardial injury in vitro and in vivo.
methodsLPS was used to induce sepsis in rats and H9c2 cells. Cardiac function of rats was assessed by an ultrasound system. Myocardial injury was revealed by hematoxylin-eosin (H&E) staining. Gain and loss of function of TTN-AS1, miR-29a, and E2F2 was achieved in H9c2 cells before LPS treatment. The expression levels of inflammatory cytokines and cTnT were monitored by ELISA. The expression levels of cardiac enzymes as well as reactive oxygen species (ROS) activity and mitochondrial membrane potential (MMP) were measured using the colorimetric method. The expression levels of TTN-AS1, miR-29a, E2F2, and apoptosis-related proteins were measured by RT-qPCR and/or western blotting. The proliferation and apoptosis of H9c2 cells were separately detected by CCK-8 and flow cytometry. Luciferase reporter assay was used to verify the targeting relationships among TTN-AS1, miR-29a and E2F2, and RIP assay was further used to confirm the binding between miR-29a and E2F2.
resultsTTN-AS1 was lowly expressed, while miR-29a was overexpressed in the cell and animal models of sepsis. Overexpression of TTN-AS1 or silencing of miR-29a reduced the expression levels of CK, CK-MB, LDH, TNF-B, IL-1B, and IL-6 in the supernatant of LPS-induced H9c2 cells, attenuated mitochondrial ROS activity, and enhanced MMP. Consistent results were observed in septic rats injected with OE-TTN-AS1. Knockdown of TTN-AS1 or overexpression of miR-29a increased LPS-induced inflammation and injury in H9c2 cells. TTN-AS1 regulated the expression of E2F2 by targeting miR-29a. Overexpression of miR-29a or inhibition of E2F2 abrogated the suppressive effect of TTN-AS1 overexpression on myocardial injury.
conclusionThis study indicates TTN-AS1 attenuates sepsis-induced myocardial injury by regulating the miR-29a/E2F2 axis and sheds light on lncRNA-based treatment of sepsis-induced cardiomyopathy.
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