ArticleJournal of cellular and molecular medicine2019
Histone deacetylase inhibitor LMK235 attenuates vascular constriction and aortic remodelling in hypertension.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
15 citing papers in PubMed, 28 citations in OpenAlex.
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- Histone deacetylase 4: A therapeutic target for cardiovascular diseases (Review).International journal of molecular medicine · 2025Review
- Histone deacetylases: Regulation of vascular homeostasis via endothelial cells and vascular smooth muscle cells and the role in vascular pathogenesis.Genes & diseases · 2024Review
- Selective inhibition of HDAC class IIA as therapeutic intervention for KMT2A-rearranged acute lymphoblastic leukemia.Communications biology · 2024Article
- Chromatin modifiers in human disease: from functional roles to regulatory mechanisms.Molecular biomedicine · 2024Review
- The role of P21-activated kinase (Pak1) in sinus node function.Journal of molecular and cellular cardiology · 2023Article
- Histone Deacetylase (HDAC) Inhibitors for the Treatment of Schistosomiasis.Pharmaceuticals (Basel, Switzerland) · 2022Review
- The CaMKII phosphorylation site Thr1604 in the CaChannels (Austin, Tex.) · 2020Article
- cando.py: Open Source Software for Predictive Bioanalytics of Large Scale Drug-Protein-Disease Data.Journal of chemical information and modeling · 2020Article
- Honokiol ameliorates angiotensin II-induced hypertension and endothelial dysfunction by inhibiting HDAC6-mediated cystathionine γ-lyase degradation.Journal of cellular and molecular medicine · 2020Article
- Histone deacetylase inhibitor CG200745 ameliorates high-fat diet-induced hypertension via inhibition of angiotensin II production.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Histone Deacetylase Inhibition Attenuates Aortic Remodeling in Rats under Pressure Overload.BioMed research international · 2020Article
- Impact of Gut Microbiome on Hypertensive Patients With Low-Salt Intake: Shika Study Results.Frontiers in medicine · 2020Article
- Histone deacetylase inhibitor LMK235 attenuates vascular constriction and aortic remodelling in hypertension.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here, we report that LMK235, a class I and histone deacetylase (HDAC6)-preferential HDAC inhibitor, reduces hypertension via inhibition of vascular contraction and vessel hypertrophy. Angiotensin II-infusion mice and spontaneously hypertensive rats (SHRs) were used to test the anti-hypertensive effect of LMK235. Daily injection of LMK235 lowered angiotensin II-induced systolic blood pressure (BP). A reduction in systolic BP in SHRs was observed on the second day when SHRs were treated with 3 mg/kg LMK235 every 3 days. However, LMK235 treatment did not affect angiotensin-converting enzyme 1 and angiotensin II receptor mRNA expression in either hypertensive model. LMK235, acting via the nitric oxide pathway, facilitated the relaxing of vascular contractions induced by a thromboxane A2 agonist in the rat aortic and mesenteric artery ring test. In addition, LMK235 increased nitric oxide production in HUVECs and inhibited the increasing of aortic wall thickness in both animal hypertensive models. LMK235 decreased the enhanced cell cycle-related genes cyclin D1 and E2F3 in angiotensin II-infusion mice and restored the decreased p21 expression. In addition, LMK235 suppressed calcium calmodulin-dependent protein kinase II (CaMKII) α, which is related to vascular smooth muscle cell proliferation. Inhibition or knockdown of HDAC5 blocked the CaMKIIα-induced cell cycle gene expression. Immunoprecipitation demonstrated that class I HDACs were involved in the inhibition of CaMKII α-induced HDAC4/5 by LMK235. We suggest that LMK235 should be further investigated for its use in the development of new therapeutic options to treat hypertension via reducing vascular hyperplasia or vasoconstriction.
Indexed as
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.