Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (577 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The muscle tissue of the heart. It is composed of striated, involuntary muscle cells (myocytes, cardiac) connected to form the contractile pump to generate blood flow.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Cardiac Muscle; Myocardia; Muscle, Cardiac; Cardiac Muscles; Muscles, Cardiac; Muscle, Heart; Heart Muscle; Heart Muscles.
Where it fits in the MeSH classification
- Broader topics
- Muscles; Heart; Muscle, Striated
- Narrower topics
- Papillary Muscles; Myoblasts, Cardiac; Myocytes, Cardiac
Related concepts
- Heart
- Myocytes
- Cardiac
Research landscape
PubMed indexes 219,017 records tagged with the MeSH heading “Myocardium” (counts retrieved 2026-10-31). 29,669 of them (13.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 99,823 records.
Reviews account for 18,887 records (8.6%) and meta-analyses for 234. Randomized controlled trials number 1,257 (0.6%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 99,823 |
| 2000-2009 | 40,151 |
| 2010-2019 | 49,374 |
| 2020 onward | 29,669 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 18,887 | 8.6% |
| Meta-analyses | 234 | 0.1% |
| Randomized controlled trials | 1,257 | 0.6% |
Method: PubMed query "Myocardium"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| An Outflow Tract Myocardium-Specific Enhancer at the Sema3c Locus During Heart Development | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42323952 · DOI · PMC13283761 |
| Histaminylation alters collagen matrix mechanics and attenuates cardiac fibrosis post-myocardial infarction via mechanotransduction signaling axis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42270610 · DOI · PMC13254370 |
| Selective expansion of cardiac macrophage subtypes distinguishes their functional roles in disease and homeostasis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42262886 · DOI · PMC13430008 |
An Outflow Tract Myocardium-Specific Enhancer at the Sema3c Locus During Heart Development [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Sema3c is specifically expressed in the cardiac outflow tract (OFT) of the developing mouse heart and has been implicated in OFT polarization and great artery formation.
- Closing excerpt
- This enhancer provides insight into the mechanisms underlying spatially restricted Sema3c expression involved in OFT development.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (142 words)
Sema3c is specifically expressed in the cardiac outflow tract (OFT) of the developing mouse heart and has been implicated in OFT polarization and great artery formation. However, the regulatory basis underlying its spatially restricted expression remains unclear. To investigate the mechanisms underlying OFT-specific Sema3c expression, we utilized chromatin accessibility data from distinct segments of the developing heart and identified a differentially accessible region as an OFT-specific Sema3c enhancer candidate. Unlike previously characterized Sema3c enhancers, this region is located distal to the transcription start site. Reporter analysis using transgenic mouse embryos demonstrated that this region exhibits transcriptional activity from E8.5 onward and remains specifically active in the OFT myocardium throughout heart development. We further defined a minimal 603 bp enhancer whose activity depends on GATA binding sites. This enhancer provides insight into the mechanisms underlying spatially restricted Sema3c expression involved in OFT development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42323952 · DOI · PMC13283761
Histaminylation alters collagen matrix mechanics and attenuates cardiac fibrosis post-myocardial infarction via mechanotransduction signaling axis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Histaminylation is a newly discovered monoaminylation catalyzed by transglutaminase 2 (TGM2), and its role in myocardial fibrosis has not yet been elucidated.
- Closing excerpt
- This study also highlights a novel role of histamine in maintaining stress environment mechanical stability.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (245 words)
Histaminylation is a newly discovered monoaminylation catalyzed by transglutaminase 2 (TGM2), and its role in myocardial fibrosis has not yet been elucidated. Here, we identified histaminylation in cardiac type I collagen isolated from mice 7 days after acute myocardial infarction (AMI) by mass spectrometry. Using histamine-deficient Hdc-/- mice, we demonstrated an increase in TGM2-mediated γ-glutamyl-ε-lysine crosslinks and a higher myocardial Young's modulus in the scar region of Hdc-/- mice than in wild-type controls, indicating that histaminylation might restrain the role of TGM2 in cardiac fibrogenesis after AMI. Furthermore, we reconstituted an in vitro crosslinking system, yielding unmodified collagen and histaminylated collagen. The results of mechanical indentation and electron microscopy demonstrated that histaminylation could reduce crosslink formation, lower matrix stiffness, and alter viscoelasticity. Subsequently, primary murine cardiac fibroblasts were cultured under cyclic stretch with TGF-β on different substrates, and the results revealed that histaminylated collagen strongly attenuated TGF-β-induced fibroblast-to-myofibroblast transition and reduced focal adhesion assembly. Mechanically, integrated single-cell and bulk RNA-seq analyses indicated that the PIEZO1/ITGB1 mechanotransduction axis was upregulated and mediated downstream signal transduction in the infarcted hearts of Hdc-/- mice. Finally, local delivery of a histamine-releasing hydrogel to Hdc-/- mice after AMI could significantly reinstate collagen histaminylation and reduce crosslink abundance and cardiac dysfunction. Collectively, these data reveal that collagen histaminylation limits TGM2-dependent crosslinking, softens the extracellular matrix, and inhibits the PIEZO1/ITGB1 axis, thereby mitigating myocardial fibrosis after AMI. This study also highlights a novel role of histamine in maintaining stress environment mechanical stability.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42270610 · DOI · PMC13254370
Selective expansion of cardiac macrophage subtypes distinguishes their functional roles in disease and homeostasis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Cardiac macrophages are broadly studied as 2 subtypes, tissue-resident CX3C chemokine motif receptor 1 positive (CX3CR1+) that are also CC motif chemokine receptor 2 negative (CCR2-) and monocyte-derived CCR2+.
- Closing excerpt
- In conclusion, cardiac-specific selective enrichment of macrophage subtypes shows their intricate interplay and unique functional roles in regulating myocardial inflammation and fibrosis during hypertrophy and at homeostasis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (190 words)
Cardiac macrophages are broadly studied as 2 subtypes, tissue-resident CX3C chemokine motif receptor 1 positive (CX3CR1+) that are also CC motif chemokine receptor 2 negative (CCR2-) and monocyte-derived CCR2+. Previous systemic loss-of-function approaches suggested unique roles for each subtype in the heart, with CCR2+ being inflammatory and CX3CR1+ being prohealing. Here, we employed a cardiac-specific gain-of-function approach to selectively enhance either macrophage subtype. A robust increase in basal CCR2+ macrophages in the heart by targeted CC chemokine ligand 2 (Ccl2) expression did not induce inflammation, cause fibroblast activation, or impair cardiac function. However, increased CCR2+ macrophages reciprocally diminished self-renewing tissue-resident macrophages and worsened cardiac fibrosis due to pressure overload stimulation. Conversely, augmented expression of colony-stimulating factor-1 (Csf1) in the heart promoted selective expansion of resident CX3CR1+ macrophages, which exerted no pathophysiological consequences at steady state. However, pressure overload in these mice with expanded CX3CR1+ macrophages showed a CCR2+ macrophage-dependent inflammation leading to exacerbated cardiac dysfunction, simultaneously protecting from adverse remodeling and cardiac fibrosis. In conclusion, cardiac-specific selective enrichment of macrophage subtypes shows their intricate interplay and unique functional roles in regulating myocardial inflammation and fibrosis during hypertrophy and at homeostasis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42262886 · DOI · PMC13430008
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Effect of microvascular obstruction and intramyocardial hemorrhage by CMR on LV remodeling and outcomes after myocardial infarction: a systematic review and meta-analysis [4]
- Research article Prognostic Value of Myocardial Scarring on CMR in Patients With Cardiac Sarcoidosis [5]
- Research article Presence of Late Gadolinium Enhancement by Cardiac Magnetic Resonance Among Patients With Suspected Cardiac Sarcoidosis Is Associated With Adverse Cardiovascular Prognosis: A Systematic Review and Meta-Analysis [6]
- Research article Histologic validation of myocardial fibrosis measured by T1 mapping: a systematic review and meta-analysis [7]
- Research article Native T1 Mapping, Extracellular Volume Mapping, and Late Gadolinium Enhancement in Cardiac Amyloidosis: A Meta-Analysis [8]
- Research article Prognostic Impact of Late Gadolinium Enhancement by Cardiovascular Magnetic Resonance in Myocarditis: A Systematic Review and Meta-Analysis [9]
References
- Wang Y, Harada Y, Ueyama T, Seya D, Nakagawa O, Kawamura T. An Outflow Tract Myocardium-Specific Enhancer at the Sema3c Locus During Heart Development. . 2026. PMID 42323952 · DOI · PMC13283761
- Zhu J, Sun D, Zeng G, Wu K, Yang X, Zhu X, et al.. Histaminylation alters collagen matrix mechanics and attenuates cardiac fibrosis post-myocardial infarction via mechanotransduction signaling axis. . 2026. PMID 42270610 · DOI · PMC13254370
- Kasam RK, Vagnozzi RJ, Kuwabara Y, Johansen AKZ, Blair NS, Prasad V, et al.. Selective expansion of cardiac macrophage subtypes distinguishes their functional roles in disease and homeostasis. . 2026. PMID 42262886 · DOI · PMC13430008
- Hamirani YS, Wong A, Kramer CM, Salerno M. Effect of microvascular obstruction and intramyocardial hemorrhage by CMR on LV remodeling and outcomes after myocardial infarction: a systematic review and meta-analysis. JACC Cardiovasc Imaging. 2014. PMID 25212800 · DOI · PMC4301583
- Coleman GC, Shaw PW, Balfour PC, Gonzalez JA, Kramer CM, Patel AR, et al.. Prognostic Value of Myocardial Scarring on CMR in Patients With Cardiac Sarcoidosis. JACC Cardiovasc Imaging. 2017. PMID 27450877 · DOI · PMC5237422
- Hulten E, Agarwal V, Cahill M, Cole G, Vita T, Parrish S, et al.. Presence of Late Gadolinium Enhancement by Cardiac Magnetic Resonance Among Patients With Suspected Cardiac Sarcoidosis Is Associated With Adverse Cardiovascular Prognosis: A Systematic Review and Meta-Analysis. Circ Cardiovasc Imaging. 2016. PMID 27621357 · DOI · PMC5449111
- Diao KY, Yang ZG, Xu HY, Liu X, Zhang Q, Shi K, et al.. Histologic validation of myocardial fibrosis measured by T1 mapping: a systematic review and meta-analysis. J Cardiovasc Magn Reson. 2016. PMID 27955698 · DOI · PMC5154013
- Pan JA, Kerwin MJ, Salerno M. Native T1 Mapping, Extracellular Volume Mapping, and Late Gadolinium Enhancement in Cardiac Amyloidosis: A Meta-Analysis. JACC Cardiovasc Imaging. 2020. PMID 32498919 · DOI · PMC7340140
- Georgiopoulos G, Figliozzi S, Sanguineti F, Aquaro GD, di Bella G, Stamatelopoulos K, et al.. Prognostic Impact of Late Gadolinium Enhancement by Cardiovascular Magnetic Resonance in Myocarditis: A Systematic Review and Meta-Analysis. Circ Cardiovasc Imaging. 2021. PMID 33441003 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.