Evidence map›Paper›PMID 36046692›Full record

ArticleOxidative medicine and cellular longevity2022

Hyperhomocysteinemia Promotes Cardiac Hypertrophy in Hypertension.

Yawen Deng, Zhitong Li, Xiangbo An, Rui Fan, Yao Wang, Jiatian Li, Xiaolei Yang, Jiawei Liao, Yunlong Xia

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.2field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  7. Sulfide regulation and catabolism in health and disease.Signal transduction and targeted therapy · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Yawen DengInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Zhitong LiInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.ORCID https://orcid.org/0000-0002-1062-5878
Xiangbo AnDepartment of Interventional Therapy, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Rui FanInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Yao WangInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Jiatian LiInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Xiaolei YangInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.ORCID https://orcid.org/0000-0002-6132-5971
Jiawei LiaoInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.ORCID https://orcid.org/0000-0001-7584-5225
Yunlong XiaInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.ORCID https://orcid.org/0000-0001-7985-3273
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperhomocysteinemia (HHcy) is positively linked with several cardiovascular diseases; however, its role and underlying mechanisms in pathological cardiac hypertrophy are still unclear. Here, we focused on the effects and underlying mechanisms of HHcy in hypertensive cardiac hypertrophy, one of the most common and typical types of pathological cardiac hypertrophy. By a retrospective analysis of the association between HHcy and cardiac hypertrophy in a hypertensive cohort, we found that the prevalence of HHcy was higher in patients with hypertrophy and significantly associated with the presence of cardiac hypertrophy after adjusting for other conventional risk factors. In mice, HHcy induced by a methionine (2% wt/wt) diet feeding significantly promoted cardiac hypertrophy as well as cardiac inflammation and fibrosis induced by 3-week angiotensin ІІ (AngІІ) infusion (1000 ng/kg/min), while folic acid (0.006% wt/wt) supplement corrected HHcy and attenuated AngII-stimulated cardiac phenotypes. Mechanistic studies further showed that homocysteine (Hcy) exacerbated AngII-stimulated expression of Calcineurin and nuclear factor of activated T cells (NFAT), which could be attenuated by folic acid both in mice and in neonatal rat cardiomyocytes. Moreover, treatment with cyclosporin A, an inhibitor of Calcineurin, blocked Hcy-stimulated Calcineurin-NFAT signaling and hypertrophy in neonatal rat cardiomyocytes. In conclusion, our study indicates that HHcy promotes cardiac hypertrophy in hypertension, and Calcineurin-NFAT pathway might be involved in the pro-hypertrophic effect of Hcy.

Indexed as

HyperhomocysteinemiaHypertensionAnimalsCalcineurinCardiomegalyFolic AcidHomocysteineHumansMiceMyocytes, CardiacNFATC Transcription FactorsRatsRetrospective StudiesCalcineurinFolic AcidHomocysteineNFATC Transcription Factors

Identifiers

PMID36046692
PMCPMC9423973
OpenAlexW4292702965

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.