Evidence map›Paper›PMID 35474295›Full record

ReviewCell death discovery2022

Targeting NAD+: is it a common strategy to delay heart aging?

Yang Yuan, Bing Liang, Xin-Lin Liu, Wen-Jing Liu, Bing-Huan Huang, Shan-Bo Yang, Yuan-Zhen Gao, Jing-Sen Meng, Meng-Jiao Li, Ting Ye and 3 more

Open access · goldAbstract readReview
In one paragraph

Review in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Metabolic Regulation of Cardiovascular Aging.Current cardiology reports · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
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.

Yang YuanCancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.ORCID http://orcid.org/0000-0002-5552-4958
Bing Liang *Cancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.
Xin-Lin Liu *Cancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.ORCID http://orcid.org/0000-0002-6311-8984
Wen-Jing LiuCancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.
Bing-Huan HuangCancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.ORCID http://orcid.org/0000-0002-5210-996X
Shan-Bo YangCancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.
Yuan-Zhen GaoCancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.
Jing-Sen MengCancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.
Meng-Jiao LiCancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.
Ting YeCancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.
Chuan-Zhi WangCancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.
Xiao-Kun HuInterventional Medicine Center, Affiliated Hospital of Qingdao University, Qingdao, China.
Dong-Ming XingCancer Institute of The Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China. xdm_tsinghua@163.com.ORCID http://orcid.org/0000-0002-2359-0440
Qingdao University · CN

Funding

China Postdoctoral Science Foundation 2020M682120China Postdoctoral Science Foundation 2021T140356National Natural Science Foundation of China (National Science Foundation of China) 3200830
6 · The paper itself

Abstract

Heart aging is the main susceptible factor to coronary heart disease and significantly increases the risk of heart failure, especially when the aging heart is suffering from ischemia-reperfusion injury. Numerous studies with NAD+ supplementations have suggested its use in anti-aging treatment. However, systematic reviews regarding the overall role of NAD+ in cardiac aging are scarce. The relationship between NAD+ signaling and heart aging has yet to be clarified. This review comprehensively summarizes the current studies on the role of NAD+ signaling in delaying heart aging from the following aspects: the influence of NAD+ supplementations on the aging heart; the relationship and cross-talks between NAD+ signaling and other cardiac aging-related signaling pathways; Importantly, the therapeutic potential of targeting NAD+ in delaying heart aging will be discussed. In brief, NAD+ plays a vital role in delaying heart aging. However, the abnormalities such as altered glucose and lipid metabolism, oxidative stress, and calcium overload could also interfere with NAD+ function in the heart. Therefore, the specific physiopathology of the aging heart should be considered before applying NAD+ supplementations. We believe that this article will help augment our understanding of heart aging mechanisms. In the meantime, it provides invaluable insights into possible therapeutic strategies for preventing age-related heart diseases in clinical settings.

Identifiers

PMID35474295
PMCPMC9042931
OpenAlexW4224881276

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.