Details for: CL0002131

Cell ID: CL0002131

Cell Name: regular ventricular cardiac myocyte

Description: Regular cardiac myocyte of a cardiac ventricle.

Synonyms: regular cardiac muscle cell of ventricle, regular ventricular cardiac muscle fiber, ventricular myocyte, ventricular cardiac muscle cell

Selected Context(s): Overall

Gene Significance Landscape

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Score:
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Genes

Contexts:

Cell Significance Index (CSI) is uniquely calculated to reveal cell-specific gene markers. More info here

Significant Genes List

Genes with the highest and lowest Percentile Rank Scores (PRS) for regular ventricular cardiac myocyte within the selected context(s).

Gene ID: A unique numerical identifier for this specific gene.
Symbol: Shortened abbreviation or name that represents this gene.
Ensembl Gene ID: A unique identifier assigned by Ensembl for genomic data mapping.
CSI Score: A combined effect size and statistical significance measure for regular ventricular cardiac myocyte. Higher scores indicate a stronger, more significant difference in expression.
(Previously described as "Fold Change", but now represents Cliff's Delta × –log10(p).)

Gene ID: A unique numerical identifier for this specific gene.
Symbol: Shortened abbreviation or name that represents this gene.
Ensembl Gene ID: A unique identifier assigned by Ensembl for genomic data mapping.
CSI Score: A combined effect size and statistical significance measure for regular ventricular cardiac myocyte. Higher scores indicate a stronger, more significant difference in expression.
Average CSI: csi sum / gene count
Cell network configuration

This network visualizes key genes for regular ventricular cardiac myocyte. It primarily includes:
1. Top genes highly significant for this cell (Num. Top Cell Genes - based on the 'Min. CSI' setting).
2. Any additional specific 'Context Genes' you add below.
The final network is a combined view. Choose an Interaction Source (pathways or protein interactions) and optionally compare CSI scores with a Baseline Cell Type.

Maximum number of selected genes.
Select a context for the baseline cell.
Select a context for the target cell.
Target Cell for CSI:  regular ventricular cardiac myocyte (CL0002131)

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Nodes (Genes):
 Query Gene
Node size also reflects Target Cell CSI magnitude.
Node Color (Target Cell CSI in specific network):
 Very High
 High
 Medium
 Low
 Very Low
 N/A or Not Sig.
Edges (Interactions):
 STRING (Protein-Protein)
 ONTOLOGY (Shared Pathway)
 Colors vary by pathway category; default arrow applies.

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## Summary The **regular ventricular cardiac myocyte** ([regular ventricular cardiac myocyte](/details-cell/CL0002131)) is a highly specialized, terminally differentiated muscle cell responsible for the contractile force of the heart's ventricles. **Overall**, its molecular identity is defined by a unique transcriptional signature that extends beyond core contractile proteins. The high specificity of the long non-coding RNA [NEAT1](/details-gene/283131) (CSI: 14.15) suggests that nuclear architecture and post-transcriptional regulation are paramount in maintaining this cell's phenotype. Concurrently, the prominence of classic muscle-associated genes like [MYOZ2](/details-gene/51778) (CSI: 12.52) affirms its primary contractile function. Intriguingly, this cell type also exhibits a highly specific expression profile of genes typically associated with the nervous system, including GABA and glutamate receptors, pointing towards unconventional signaling mechanisms that may modulate cardiac function. ## Key Characteristics and Function The functional identity of the [regular ventricular cardiac myocyte](/details-cell/CL0002131) is underpinned by several key gene clusters that emerge from its specificity profile. * **Core Contractile and Structural Machinery:** The high significance of [MYOZ2](/details-gene/51778), a calsarcin family protein, highlights its role in tethering calcineurin to the sarcomere, thereby linking calcium signaling to gene expression and hypertrophy ([Link](https://doi.org/10.1073/pnas.260501097)). This is complemented by other structural and regulatory components such as the myosin regulatory light chain [MYL12A](/details-gene/10627) and [TRIM54](/details-gene/57159) (MuRF-3), which may integrate titin kinase and microtubule-dependent signaling pathways ([Link](https://doi.org/10.1006/jmbi.2001.4448)). * **Neurotransmitter-like Signaling Pathways:** A striking feature of this cell is the highly specific expression of multiple neurotransmitter receptors. These include the GABA-A receptor subunit [GABRB1](/details-gene/2560) and several glutamate receptors ([GRID1](/details-gene/2894), [GRM1](/details-gene/2911), [GRM8](/details-gene/2918)). While the presence of the muscarinic acetylcholine receptor [CHRM2](/details-gene/1129) is expected for parasympathetic regulation of heart rate, the unique expression of this broader suite of neuro-receptors suggests a previously underappreciated capacity for cardiomyocytes to respond to or engage in local paracrine or autocrine signaling involving GABA and glutamate. * **Transcriptional and Post-transcriptional Regulation:** The top marker, [NEAT1](/details-gene/283131), is a long non-coding RNA essential for the formation of nuclear paraspeckles. Its exceptional specificity suggests that the precise spatial organization of the nucleus and the regulation of mRNA processing are critical for maintaining the cardiomyocyte's stable, differentiated state. The antisense lncRNA [TRDN AS1](/details-gene/101927990) further underscores the importance of RNA-level regulation in these cells. * **Metabolic Regulation:** The significant expression of [PERM1](/details-gene/84808), a known downstream target of PGC-1alpha, is consistent with the immense and constant energy demand of ventricular myocytes, pointing to a specialized program for regulating mitochondrial biogenesis and oxidative capacity ([Link](https://doi.org/10.1074/jbc.m113.489674)). This is further supported by the specificity of [PHKA1](/details-gene/5255), the alpha subunit of phosphorylase kinase, which is integral to glycogenolysis for rapid energy mobilization. * **Defining by Absence (Anti-Markers):** The strong negative CSI scores for a host of ubiquitously expressed genes provide critical context. Genes involved in core cellular processes, such as the RNA-binding protein [HNRNPC](/details-gene/3183), the ubiquitin gene [UBC](/details-gene/7316), and the glycolytic enzyme [GAPDH](/details-gene/2597), are not specific markers for this cell type precisely because they are essential in nearly all cells. Similarly, the negative scores for numerous mitochondrially-encoded genes ([CYTB](/details-gene/4519), [COX1](/details-gene/4512), [ATP6](/details-gene/4508)) do not indicate a lack of mitochondria; rather, they show that high-level mitochondrial gene expression is a common feature across many metabolically active cells and is not a unique or defining characteristic of ventricular myocytes compared to other cell types. ## Clinical Significance and Contextual Roles **Overall**, the gene significance profile of the [regular ventricular cardiac myocyte](/details-cell/CL0002131) offers insights into cardiac health and disease. The high specificity of [MYOZ2](/details-gene/51778), a protein that directly interacts with the hypertrophy-associated phosphatase calcineurin ([Link](https://doi.org/10.1073/pnas.260501097)), suggests it could be a sensitive biomarker or a potential therapeutic target for pathological cardiac remodeling. Its unique expression in striated muscle makes it an attractive candidate for therapies aimed at modulating the hypertrophic response with minimal off-target effects. Perhaps most significantly, the discovery of a specific neuro-receptor signature ([GABRB1](/details-gene/2560), [GRM1](/details-gene/2911), [GRM8](/details-gene/2918)) opens new avenues for cardiovascular research. It is plausible that local, non-neuronal release of glutamate or GABA during metabolic stress or ischemia could directly act on cardiomyocytes, potentially contributing to the genesis of arrhythmias or contractile dysfunction. Pharmacological agents targeting these receptors, which are widely used in neurology, may have unexplored cardiac effects that warrant investigation. Furthermore, the role of [NEAT1](/details-gene/283131) as the top marker implies that disruptions in nuclear architecture could be an underlying factor in cardiomyopathies. Alterations in [NEAT1](/details-gene/283131) levels or paraspeckle formation may lead to a destabilization of the cardiomyocyte phenotype, contributing to disease progression. ## Potential Mechanisms and Research Directions 1. **Hypothesis: Ventricular cardiomyocytes possess a functional, non-canonical neurotransmitter sensing system that modulates cellular physiology.** * **Surprising Findings:** The highly specific expression of multiple subunits for both GABA ([GABRB1](/details-gene/2560)) and glutamate ([GRID1](/details-gene/2894), [GRM1](/details-gene/2911), [GRM8](/details-gene/2918)) receptors in a non-neuronal, contractile cell is deeply unexpected. This suggests that the role of these signaling molecules in the heart may extend beyond autonomic innervation to include direct, local regulation of myocyte function. * **Testable Questions:** Using isolated primary ventricular cardiomyocytes or hiPSC-derived cardiomyocytes, does the application of specific glutamate and GABA receptor agonists alter key physiological parameters such as calcium transient amplitude and kinetics, action potential duration, or cellular oxygen consumption rates? 2. **Hypothesis: The lncRNA [NEAT1](/details-gene/283131) functions as a master regulator of the ventricular myocyte identity by organizing nuclear paraspeckles that are essential for maintaining the cell's specialized transcriptional program.** * **Surprising Findings:** It is notable that a structural non-coding RNA, rather than a protein directly involved in contraction or ion handling, emerges as the single most specific molecular marker. This elevates the importance of higher-order nuclear organization from a housekeeping function to a defining feature of the ventricular myocyte's identity. * **Testable Questions:** Does targeted degradation or knockdown of [NEAT1](/details-gene/283131) in ventricular cardiomyocytes lead to a loss of the mature phenotype, characterized by disorganized sarcomeres, altered expression of contractile protein isoforms, and the re-expression of fetal cardiac genes?