Evidence map›Paper›PMID 35896004›Full record

ArticleAging2022

Increased cytochrome C threonine 50 phosphorylation in aging heart as a novel defensive signaling against hypoxia/reoxygenation induced apoptosis.

Fanqi Li, Haoxuan Sun, Xiaolong Lin, Qiuyu Li, Donghui Zhao, Zichao Cheng, Jinghua Liu, Qian Fan

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

Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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  3. Review
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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

8 authors at 2 institutions in 1 country.

Fanqi LiDepartment of Cardiology, Beijing An Zhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung, and Blood Vessel Disease, Beijing, China.
Haoxuan SunDepartment of Cardiology, Beijing An Zhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung, and Blood Vessel Disease, Beijing, China.
Xiaolong LinDepartment of Cardiology, Beijing An Zhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung, and Blood Vessel Disease, Beijing, China.
Qiuyu LiDepartment of Cardiology, Beijing An Zhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung, and Blood Vessel Disease, Beijing, China.
Donghui ZhaoDepartment of Cardiology, Beijing An Zhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung, and Blood Vessel Disease, Beijing, China.
Zichao ChengDepartment of Cardiology, Beijing An Zhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung, and Blood Vessel Disease, Beijing, China.
Jinghua LiuDepartment of Cardiology, Beijing An Zhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung, and Blood Vessel Disease, Beijing, China.
Qian FanDepartment of Cardiology, Beijing An Zhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung, and Blood Vessel Disease, Beijing, China.
Capital Medical University · CNBeijing Anzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have shown that aging promotes myocardial apoptosis. However, the detailed mechanisms remain unclear. Our recent studies revealed that aging not only activates apoptosis, but also activates some anti-apoptotic factors. By quantitative phosphoproteomics, here we demonstrated that aging increases cytochrome c (Cytc) phosphorylation at threonine 50 (T50), a post-translational modification with unknown functional impact. With point mutation and lentivirus transfection, cardiomyocytes were divided into four groups: empty vector group, WT (wild type), T50E (as a phosphomimic variant), and T50A (non-phosphorylatable). TUNEL staining and flow cytometry were used to determine the apoptosis ratio in different groups after hypoxic/reoxygenated (H/R) treatment. The results showed that T50-phosphorylated Cytc suppressed myocardial apoptosis induced by H/R. Furthermore, Western Blot and ELISA measurements revealed that Cytc T50 phosphorylation inhibited caspase-9 and caspase-3 activity without altering caspase-8, BCL-2, BCL-XL, and Bax expression. In our study, we demonstrated that aging increases phosphorylation Cytc at T50 and this aging-increasing phosphorylation site can suppress H/R-induced apoptosis.

Indexed as

Cytochromes cThreonineAgingApoptosisHumansHypoxiaMyocytes, CardiacPhosphorylationCytochromes cThreonineagingapoptosishypoxic/reoxygenated injuryphosphorylation

Identifiers

PMID35896004
PMCPMC9365549
OpenAlexW4287832076

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.