SynthesisCells2022
A Systemic Review of the Integral Role of TRPM2 in Ischemic Stroke: From Upstream Risk Factors to Ultimate Neuronal Death.
Synthesis in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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.
Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- Sinapic Acid Reduces Hypoxia-Induced Cell Damage in Hep-2 Cells by Regulating TRPM2 Channel Activation.Journal of biochemical and molecular toxicology · 2026Article
- Mismatch-time ratio combined with ASPECTS: a novel indicator of favorable prognosis in multimodal ct prediction of anterior circulation large vessel occlusion.BMC neurology · 2026Article
- Molecular Mechanisms and Targeted Intervention Strategies of Calcium Overload in Ischemic Stroke.International journal of molecular sciences · 2026Review
- Neuroimmune Regulation by TRPM2 Channels.Cells · 2026Review
- TRPM2: a pivotal player in tumor progression and a promising therapeutic target.Cancer cell international · 2025Review
- Reactive Oxygen Species-Mediated TRPM2 Activation Facilitates Phagocytosis of Macrophages to Reverse Profibrotic Phenotype.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
- Dynamic changes in BDNF, VEGF, and GDNF after transplanting human protein-based scaffolds with Wharton's Jelly MSCs in a rat brain injury model.Scientific reports · 2025Article
- TRPM2 overactivation drives hyperlipidemia-induced dysfunction of myeloid cells and neurovascular units.Cell reports. Medicine · 2025Article
- TRP Channels in Excitotoxicity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- Uncovering a new mechanism of ischemic stroke: a study of the association between γδ T cells and immunoinflammation.Frontiers in immunology · 2025Review
- [Construction of HEK293T cell line stably expressing TRPM2 channel based on PiggyBac transposition system and its application in drug screening for cerebral ischemia and other diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Article
- TRP Channels in Stroke.Neuroscience bulletin · 2024Review
- Whole-genome sequencing identifies variants in ANK1, LRRN1, HAS1, and other genes and regulatory regions for stroke in type 1 diabetes.Scientific reports · 2024Article
- TRPM2 enhances ischemic excitotoxicity by associating with PKCγ.Cell reports · 2024Article
- Targeting TRPM2- and TRPM4-extrasynaptic N-methyl-D-aspartate receptor coupling in ischemic stroke.Neural regeneration research · 2023Article
- TRPM2-mediated CaCell communication and signaling : CCS · 2023Review
- TRP Channels in Oxidative Stress Signalling.Cells · 2023Article
- TRPM2: bridging calcium and ROS signaling pathways-implications for human diseases.Frontiers in physiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Ischemic stroke causes a heavy health burden worldwide, with over 10 million new cases every year. Despite the high prevalence and mortality rate of ischemic stroke, the underlying molecular mechanisms for the common etiological factors of ischemic stroke and ischemic stroke itself remain unclear, which results in insufficient preventive strategies and ineffective treatments for this devastating disease. In this review, we demonstrate that transient receptor potential cation channel, subfamily M, member 2 (TRPM2), a non-selective ion channel activated by oxidative stress, is actively involved in all the important steps in the etiology and pathology of ischemic stroke. TRPM2 could be a promising target in screening more effective prophylactic strategies and therapeutic medications for ischemic stroke.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.