ArticleJournal of cellular and molecular medicine2020
HDAC1-mediated deacetylation of LSD1 regulates vascular calcification by promoting autophagy in chronic renal failure.
Article in Journal of cellular and molecular medicine, 2020. 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, 17 citations in OpenAlex.
- The Protective Effects of the Autophagic and Lysosomal Machinery in Vascular and Valvular Calcification: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- Identification and validation of programmed cell death-related genes in osteosarcoma: inhibiting CIB1 as a promising therapeutic strategy.BMC cancer · 2026Article
- A novel deacetylase inhibitor KLX suppresses liver fibrosis by deacetylating PPARγ through promoting ubiquitination-mediated HDAC1 degradation.Science China. Life sciences · 2025Article
- Review
- Histone demethylases in autophagy and inflammation.Cell communication and signaling : CCS · 2025Review
- Oxidative stress and its related epigenetic modifications in vascular calcification: mechanisms and advances.Frontiers in cardiovascular medicine · 2025Review
- Mechanism of HDAC1 Regulating Iron Overload-Induced Neuronal Oxidative Damage After Cerebral Hemorrhage.Molecular neurobiology · 2024Article
- Vascular Calcification: In Vitro Models under the Magnifying Glass.Biomedicines · 2022Review
- Quercetin alleviates chronic renal failure by targeting the PI3k/Akt pathway.Bioengineered · 2021Article
- Genetic Variants and Functional Analyses of theFrontiers in genetics · 2021Article
- HDAC1-mediated deacetylation of LSD1 regulates vascular calcification by promoting autophagy in chronic renal failure.Journal of cellular and molecular medicine · 2020Article
- SESTRINs: Emerging Dynamic Stress-Sensors in Metabolic and Environmental Health.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic renal failure (CRF) is commonly associated with various adverse consequences including pathological vascular calcification (VC), which represents a significant clinical concern. Existing literature has suggested the involvement of histone deacetylases (HDACs) in the progression of CRF-induced VC. However, the underlying molecular mechanisms associated with HDACs remain largely unknown. Therefore, we established the adenine-induced CRF rat model and in vitro VC models based on vascular smooth muscle cells (VSMCs) to examine HDAC1/lysine demethylase 1A (LSD1)/SESN2 as a novel molecular pathway in CRF-induced VC. Our initial results demonstrated that HDAC1 reduced the formation of VC in vivo and in vitro. HDAC1 was found to deacetylate LSD1, which subsequently led to impaired transcriptional activity in CRF-induced VC. Moreover, our results illustrated that LSD1 diminished the enrichment of H3K4me2 at the SESN2 promoter. Autophagy was identified as a vasculo-protective element against calcification in VC. Finally, we found that the inhibitory effects of HDAC1 overexpression on VC were partially abolished via over-expressed LSD1 in adenine-induced CRF model rats and in high phosphate-induced VSMCs. Taken together, these results highlight the crucial role of HDAC1 as an antagonistic factor in the progression of VC in CRF, and also revealed a novel regulatory mechanism by which HDAC1 operates. These findings provide significant insight and a fresh perspective into promising novel treatment strategies by up-regulating HDAC1 in CRF.
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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.