Evidence map›Paper›PMID 30527623›Full record

ArticleEBioMedicine2019

Heme oxygenase-1 prevents heart against myocardial infarction by attenuating ischemic injury-induced cardiomyocytes senescence.

Huitong Shan, Tianyu Li, Lijia Zhang, Rui Yang, Yue Li, Mingyu Zhang, Yuechao Dong, Yuhong Zhou, Chaoqian Xu, Baofeng Yang and 3 more

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

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

45 citing papers in PubMed, 69 citations in OpenAlex.

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  15. Unraveling the Roles of HIF-1, HO-1, GLUT-1 and GLUT-4 in Myocardial Protection.International journal of drug discovery and pharmacology · 2024
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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

13 authors at 1 institution in 1 country.

Huitong ShanDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China; Northern Translational Medicine Research and Cooperation Center, Heilongjiang Academy of Medical Sciences, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
Tianyu LiDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China; Northern Translational Medicine Research and Cooperation Center, Heilongjiang Academy of Medical Sciences, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
Lijia ZhangDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
Rui YangDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
Yue LiDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China; Northern Translational Medicine Research and Cooperation Center, Heilongjiang Academy of Medical Sciences, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
Mingyu ZhangDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
Yuechao DongDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China; Northern Translational Medicine Research and Cooperation Center, Heilongjiang Academy of Medical Sciences, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
Yuhong ZhouDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
Chaoqian XuDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China; Department of Pharmacology, Mudanjiang Medical University, Mudanjiang 157011, People's Republic of China.
Baofeng YangDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
Haihai LiangDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China; Northern Translational Medicine Research and Cooperation Center, Heilongjiang Academy of Medical Sciences, Harbin Medical University, Harbin, Heilongjiang 150081, PR China. Electronic address: lianghaihai@ems.hrbmu.edu.cn.
Xu GaoNorthern Translational Medicine Research and Cooperation Center, Heilongjiang Academy of Medical Sciences, Harbin Medical University, Harbin, Heilongjiang 150081, PR China; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang 150081, PR China; Key Laboratory of Cardiovascular Medicine Research of Harbin Medical University, Ministry of Education, Harbin, PR China. Electronic address: gaoxu@hrbmu.edu.cn.
Hongli ShanDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China; Northern Translational Medicine Research and Cooperation Center, Heilongjiang Academy of Medical Sciences, Harbin Medical University, Harbin, Heilongjiang 150081, PR China. Electronic address: shanhongli@ems.hrbmu.edu.cn.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCellular senescence is a stable cell-cycle arrest induced by telomere shortening and various types of cellular stress including oxidative stress, oncogene activation, DNA damage etc. Heme oxygenase-1 (HO-1) is an inducible stress-response protein that plays antioxidant and anti-apoptotic effects. However, the role and underlying mechanisms of HO-1 in cellular senescence in heart are largely unknown.

methodsEchocardiography was employed to detect the effect of HO-1 on heart function in adult mice with myocardial infarction (MI) and aged mice. The senescence markers, p53, p16 and LaminB, were analyzed by western blot. The immunofluorescence and immunohistochemical staining were applied to analyze the expression level of p16. SA-β-Gal staining showed the level of cardiomyocyte senescence.

findingsWe found that hemin significantly induced the expression of HO-1, which notably suppressed cardiomyocyte senescence containing the secretion of senescence-associated secretory phenotype. Further studies showed that systemic HO-1 transgenic overexpression improved heart function by inhibiting aging-induced extracellular matrix deposition and fibrogenesis. More importantly, treatment of hemin improved heart function in MI mice. Furthermore, forced expression of HO-1 blunted cardiomyocyte senescence in natural aged mice and in primary cultured neonatal mouse cardiomyocytes.

interpretationOur study revealed that HO-1 improved heart function and attenuated cardiomyocyte senescence triggered by ischemic injury and aging. In addition, HO-1 induction alleviated H

Indexed as

AgingAnimalsAnimals, Genetically ModifiedBiomarkersCells, CulturedCellular SenescenceDisease Models, AnimalExtracellular MatrixGene Expression RegulationHeme Oxygenase-1HeminHydrogen PeroxideMaleMiceMyocardial InfarctionMyocytes, CardiacBiomarkersHeme Oxygenase-1HeminHMOX1 protein, humanHydrogen PeroxideExtracellular matrixHeme oxygenase-1Myocardial infarctionSenescenceSenescence-associated secretory phenotype

Identifiers

PMID30527623
PMCPMC6355645
OpenAlexW2903210098

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.