Evidence map›Paper›PMID 37654208›Full record

ReviewInternational journal of molecular medicine2023

Role of RIPK3‑CaMKII‑mPTP signaling pathway‑mediated necroptosis in cardiovascular diseases (Review).

Sheng Chen, Senhong Guan, Zhaohan Yan, Fengshan Ouyang, Shuhuan Li, Lanyuan Liu, Jiankai Zhong

Open access · hybridAbstract readReview
In one paragraph

Review in International journal of molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
  4. A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

7 authors at 2 institutions in 1 country.

Sheng ChenDepartment of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, Guangdong 528308, P.R. China.
Senhong GuanDepartment of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, Guangdong 528308, P.R. China.
Zhaohan YanDepartment of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, Guangdong 528308, P.R. China.
Fengshan OuyangDepartment of Rehabilitation Medicine, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, Guangdong 528308, P.R. China.
Shuhuan LiDepartment of Pediatrics, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, Guangdong 528308, P.R. China.
Lanyuan LiuDepartment of Ultrasound Medicine, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, Guangdong 528308, P.R. China.
Jiankai ZhongDepartment of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, Guangdong 528308, P.R. China.
The First People's Hospital of Shunde · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Necroptosis, which is distinct from apoptosis and necrosis, serves a crucial role in ontogeny and the maintenance of homeostasis. In the last decade, it has been demonstrated that the pathogenesis of cardiovascular diseases is also linked to necroptosis. Receptor interaction protein kinase (RIPK) 1, RIPK3 and mixed lineage kinase domain‑like protein serve vital roles in necroptosis. In addition to the aforementioned necroptosis‑related components, calcium/calmodulin‑dependent protein kinase II (CaMKII) has been identified as a novel substrate for RIPK3 that promotes the opening of the mitochondrial permeability transition pore (mPTP), and thus, mediates necroptosis of myocardial cells through the RIPK3‑CaMKII‑mPTP signaling pathway. The present review provides an overview of the current knowledge of the RIPK3‑CaMKII‑mPTP‑mediated necroptosis signaling pathway in cardiovascular diseases, focusing on the role of the RIPK3‑CaMKII‑mPTP signaling pathway in acute myocardial infarction, ischemia‑reperfusion injury, heart failure, abdominal aortic aneurysm, atherosclerosis, diabetic cardiomyopathy, hypertrophic cardiomyopathy, atrial fibrillation, and the cardiotoxicity associated with antitumor drugs and other chemicals. Finally, the present review discusses the research status of drugs targeting the RIPK3‑CaMKII‑mPTP signaling pathway.

Indexed as

Cardiovascular DiseasesHeart FailureCalcium-Calmodulin-Dependent Protein Kinase Type 2HumansNecroptosisReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionCalcium-Calmodulin-Dependent Protein Kinase Type 2Receptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humanCaMKIIcardiovascular diseasesdrug targetmPTPnecroptosisRIPK3

Identifiers

PMID37654208
PMCPMC10495754
OpenAlexW4386293374

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.