ArticleCell death discovery2022
Anti-fibrotic mechanism of SPP1 knockdown in atrial fibrosis associates with inhibited mitochondrial DNA damage and TGF-β/SREBP2/PCSK9 signaling.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Kidney fibrosis molecular mechanisms Spp1 influences fibroblast activity through transforming growth factor beta smad signaling.iScience · 2024Article
- The Role of Biochemical Cardiac Markers in Atrial Fibrillation.The Journal of innovations in cardiac rhythm management · 2023Review
- Identifying Fibrogenic Cells Following Salivary Gland Obstructive Injury.bioRxiv : the preprint server for biology · 2023Article
- Identifying fibrogenic cells following salivary gland obstructive injury.Frontiers in cell and developmental biology · 2023Article
- Downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis.Biology direct · 2022Article
- Clinical and Molecular Implications of Osteopontin in Heart Failure.Current issues in molecular biology · 2022Review
Corrections and comments
- Retraction · 2023-06-30Error in Data · Error in Image ·
- Retracted
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrosis occurs frequently with structural heart disease and is considered as a major cause of arrhythmia. Microarray-based profiling predicted the differential expression of SPP1 in atrial fibrosis. Herein, we aimed to analyze the role of shRNA-mediated SPP1 knockdown in the progression of atrial fibrosis as well as the downstream mechanism. In vivo model in mice and in vitro HL-1 cell model of atrial fibrosis were developed by the angiotensin II (Ang II) method, where SPP1 expression was validated by RT-qPCR. Gain- and loss-of-function experiments were performed in Ang II-induced mice and HL-1 cells to evaluate the effect of the SPP1/TGF-β/SREBP2/PCSK9 axis on cell viability, apoptosis, collagen production and mitochondrial DNA (mtDNA) damage in atrial fibrosis. Expression of SPP1, TGF-β, SREBP2 and PCSK9 was increased in Ang II-induced mice and HL-1 cells. Silencing of SPP1 inhibited the occurrence of atrial fibrosis, as reflected by attenuated cell viability and collagen production as well as increased cell apoptosis. Conversely, upregulated SPP1 enhanced atrial fibrosis, which was related to upregulation of TGF-β. In addition, TGF-β elevated the expression of SREBP2, which promoted mtDNA damage and the consequent atrial fibrosis by augmenting the expression of PCSK9. This study uncovers previously unrecognized pro-fibrotic activities of SPP1 in atrial fibrosis, which is achieved through activation of the TGF-β/SREBP2/PCSK9 signaling pathway and promotion of mtDNA damage.
Identifiers
What 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.