Evidence map›Paper›PMID 36771298›Full record

ReviewNutrients2023

Targeting Iron Metabolism and Ferroptosis as Novel Therapeutic Approaches in Cardiovascular Diseases.

Yufei Chen, Xueting Li, Siyuan Wang, Ran Miao, Jiuchang Zhong

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
29.5field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 114 citations in OpenAlex.

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  20. The role of ferroptosis in vascular endothelial cells and its role in the pathogenesis of cervical spondylosis of vertebral artery type: a comprehensive review.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026
    Review

21 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Yufei ChenHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Xueting LiHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Siyuan WangHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Ran MiaoMedical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Jiuchang ZhongHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.ORCID 0000-0002-2315-3515
Capital Medical University · CN

Funding

Beijing Natural Science Foundation 7222068Clinical Research Incubation Program of Beijing Chaoyang Hospital Affiliated to Capital Medi-cal University CYFH202209General Program and the National Major Research Plan Training Program of the National Nat-ural Science Foundation of China 92168117; 81770253; 91849111Reform and Development Program of Beijing Institute of Respiratory Medicine ysrh2022002
6 · The paper itself

Abstract

Iron functions as an essential micronutrient and participates in normal physiological and biochemical processes in the cardiovascular system. Ferroptosis is a novel type of iron-dependent cell death driven by iron accumulation and lipid peroxidation, characterized by depletion of glutathione and suppression of glutathione peroxidase 4 (GPX4). Dysregulation of iron metabolism and ferroptosis have been implicated in the occurrence and development of cardiovascular diseases (CVDs), including hypertension, atherosclerosis, pulmonary hypertension, myocardial ischemia/reperfusion injury, cardiomyopathy, and heart failure. Iron chelators deferoxamine and dexrazoxane, and lipophilic antioxidants ferrostatin-1 and liproxstatin-1 have been revealed to abolish ferroptosis and suppress lipid peroxidation in atherosclerosis, cardiomyopathy, hypertension, and other CVDs. Notably, inhibition of ferroptosis by ferrostatin-1 has been demonstrated to alleviate cardiac impairments, fibrosis and pathological remodeling during hypertension by potentiating GPX4 signaling. Administration of deferoxamine improved myocardial ischemia/reperfusion injury by inhibiting lipid peroxidation. Several novel small molecules may be effective in the treatment of ferroptosis-mediated CVDs. In this article, we summarize the regulatory roles and underlying mechanisms of iron metabolism dysregulation and ferroptosis in the occurrence and development of CVDs. Targeting iron metabolism and ferroptosis are potential therapeutic strategies in the prevention and treatment of hypertension and other CVDs.

Indexed as

Cardiovascular DiseasesFerroptosisHypertensionMyocardial Reperfusion InjuryCyclohexylaminesDeferoxamineHumansIronLipid PeroxidationPhenylenediaminesCyclohexylaminesDeferoxamineferrostatin-1IronPhenylenediaminescardiovascular diseasesferroptosisiron chelatoriron metabolismlipid peroxidation

Identifiers

PMID36771298
PMCPMC9921472
OpenAlexW4317810550

What OpenQuestion holds

Textmetadata
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.