ArticleInternational journal of clinical and experimental pathology2020
MiR-144 affects proliferation and apoptosis of high glucose-induced AC16 cardiomyocytes by regulating CTRP3/JNK signaling.
Article in International journal of clinical and experimental pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- From Type 2 Diabetes Mellitus To Diabetic Cardiomyopathy - A Systematic Review On The Role Of MicroRNA.Current diabetes reports · 2025Pooled it
- Multifunctional Roles and Therapeutic Prospects of C1q/TNF-Related Protein 3 (CTRP3) in Human Diseases.Current medical science · 2025Review
- The interregulatory circuit between non-coding RNA and apoptotic signaling in diabetic cardiomyopathy.Non-coding RNA research · 2024Review
- Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024Review
- Circulating microRNAs and cardiomyocyte proliferation in heart failure patients related to 10 years survival.ESC heart failure · 2023Article
- A novel identified circular RNA, circSnap47, promotes heart failure progression via regulation of miR-223-3p/MAPK axis.Molecular and cellular biochemistry · 2023Article
- CTRP3 attenuates inflammation, oxidative and cell death in cisplatin induced HK-2 cells.PeerJ · 2023Article
- Plasma miR-409-3p promotes acute cerebral infarction via suppressing CTRP3.The Kaohsiung journal of medical sciences · 2021Article
- Molecular Mechanisms and Epigenetic Regulation in Diabetic Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Review
- The CTRP3-AdipoR2 Axis Regulates the Development of Experimental Autoimmune Encephalomyelitis by Suppressing Th17 Cell Differentiation.Frontiers in immunology · 2021Article
- New Insights Into Implications of CTRP3 in Obesity, Metabolic Dysfunction, and Cardiovascular Diseases: Potential of Therapeutic Interventions.Frontiers in physiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic cardiomyopathy (DCM) is a common complication of diabetes and can lead to heart failure, arrhythmia, and sudden death. microRNAs (miRNAs) are reportedly involved in many human disease, including DCM. However, little is known about the biologic functions of miR-144 in DCM progression.
methodsThe expression levels of miR-144 and C1q/TNF-related protein-3 (CTRP3) were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Western blot was used to determine the protein levels of CTRP3, phosphorylated c-Jun amino-terminal kinase (p-JNK), JNK, Bax, Bcl-2, and cleaved-caspase-3. Cell proliferation and apoptosis were detected by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The potential binding sites between miR-144 and CTRP3 were predicted by microRNA.org databases and further determined using a dual-luciferase assay. AC16 cardiomyocytes were cultured in high glucose (HG, 30 mmol/L) to mimic hyperglycemia.
resultsMiR-144 expression level was enhanced, while CTRP3 expression was reduced in HG-induced AC16 cardiomyocytes. Knockdown of miR-144 or overexpression of CTRP3 dramatically promoted cell proliferation and reduced apoptosis of AC16 cardiomyocytes treated with HG. Inhibition of miR-144 evidently decreased the protein levels of Bax and p-JNK, but elevated Bcl-2 expression in HG-induced AC16 cardiomyocytes. Moreover, CTRP3 was a direct target of miR-144, and its abrogation reversed the effects of miR-144 knockdown on proliferation and apoptosis in HG-induced AC16 cardiomyocytes. SP600125 (a JNK inhibitor, 10 μmol/L) attenuated the si-CTRP3-mediated inhibition of proliferation and promotion of apoptosis in AC16 cardiomyocytes transfected with anti-miR-144 and stimulated with HG.
conclusionMiR-144 regulates proliferation and apoptosis of HG-induced AC16 cardiomyocytes through targeting the CTRP3/JNK signaling pathway, providing a novel avenue for treatment of DCM.
Indexed as
Identifiers
32211094PMC7061800W3013322819What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.