ArticlePloS one2012
MAPK signaling drives inflammation in LPS-stimulated cardiomyocytes: the route of crosstalk to G-protein-coupled receptors.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 60 citations in OpenAlex.
- Research Progress on the Role of Traditional Chinese Medicine in Regulating Ferroptosis in Cardiovascular Diseases.Biology · 2026Review
- Race and Sex Differences in PRMT6 Expression in Lung Tumors in Relation to Neighborhood Violence.Cancer prevention research (Philadelphia, Pa.) · 2025Article
- Unravelling butyrate metabolism in sepsis: identification of key genes.BMC infectious diseases · 2025Article
- Targeting ATF4-DDIT4/TXNIP induced mitochondrial dysfunction and ferroptosis: ISRIB as novel therapy for septic cardiomyopathy.Journal of translational medicine · 2025Article
- Kehuang capsule inhibits MAPK and AKT signaling pathways to mitigate CClLiver research (Beijing, China) · 2024Article
- Boron in wound healing: a comprehensive investigation of its diverse mechanisms.Frontiers in bioengineering and biotechnology · 2024Review
- Effect of miR-412-5p-loaded exosomes in H9c2 cardiomyocytes via the MAPK pathway.Iranian journal of basic medical sciences · 2024Article
- SGLT2 Inhibitors in Aging-Related Cardiovascular Disease: A Review of Potential Mechanisms.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway.Scientific reports · 2023Article
- Hesperetin attenuates LPS-induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway.Immunity, inflammation and disease · 2023Article
- Review
- Multifaceted role of ferroptosis in cardiovascular disease.Acta biochimica et biophysica Sinica · 2023Review
- Integration of transcriptomic, proteomic, and metabolomic data to identify lncRNA rPvt1 associations in lipopolysaccharide-treated H9C2 cardiomyocytes.Frontiers in genetics · 2023Article
- Identification of two novel ferroptosis-associated targets in sepsis-induced cardiac injury: Hmox1 and Slc7a11.Frontiers in cardiovascular medicine · 2023Article
- Inhibition of ferroptosis alleviates high-power microwave-induced myocardial injury.Frontiers in cardiovascular medicine · 2023Article
- Reactive metal boride nanoparticles trap lipopolysaccharide and peptidoglycan for bacteria-infected wound healing.Nature communications · 2022Article
- Short-term transcriptomic response to plasma membrane injury.Scientific reports · 2021Article
- Multiomics characteristics of neurogenesis-related gene are dysregulated in tumor immune microenvironment.NPJ genomic medicine · 2021Article
- PH-responsive strontium nanoparticles for targeted gene therapy against mammary carcinoma cells.Asian journal of pharmaceutical sciences · 2021Article
- Ferroptosis Is a Potential Novel Diagnostic and Therapeutic Target for Patients With Cardiomyopathy.Frontiers in cell and developmental biology · 2021Review
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 2 institutions in 1 country.
Funding
Abstract
Profound cardiovascular dysfunction is an important cause of mortality from septic shock. The molecular underpinnings of cardiac dysfunction during the inflammatory surge of early sepsis are not fully understood. MAPKs are important signal transducers mediating inflammation whereas G-protein signaling pathways modulate the cardiac response to stress. Using H9c2 cardiomyocytes, we investigated the interaction of MAPK and G-protein signaling in a sepsis model to test the hypothesis that the cardiomyocyte inflammatory response is controlled by MAPKs via G-protein-mediated events. We found that LPS stimulated proinflammatory cytokine production was markedly exacerbated by siRNA knockdown of the MAPK negative regulator Mkp-1. Cytokine production was blunted when cells were treated with p38 inhibitor. Two important cellular signaling molecules typically regulated by G-protein-coupled receptors, cAMP and PKC activity, were also stimulated by LPS and inflammatory cytokines TNF-α and IL-6, through a process regulated by Mkp-1 and p38. Interestingly, neutralizing antibodies against Gα(s) and Gα(q) blocked the increase in cellular cAMP and PKC activation, respectively, in response to inflammatory stimuli, indicating a critical role of G-protein coupled receptors in this process. LPS stimulation increased COX-2 in H9c2 cells, which also express prostaglandin receptors. Blockade of G-protein-coupled EP4 prostaglandin receptor by AH 23848 prevented LPS-induced cAMP increase. These data implicate MAPKs and G-proteins in the cardiomyocyte inflammatory response to LPS as well as crosstalk via COX-2-generated PGE(2). These data add to our understanding of the pathogenesis of septic shock and have the potential to guide the selection of future therapeutics.
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.