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: 4 complete abstracts (739 words), 10 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 geometric and structural changes that the heart ventricles undergo, usually following myocardial infarction. It comprises expansion of the infarct and dilatation of the healthy ventricle segments. While most prevalent in the left ventricle, it can also occur in the right ventricle.
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: Remodelings, Ventricular; Remodeling, Ventricular; Ventricular Remodelings; Cardiac Remodeling, Ventricular; Cardiac Remodelings, Ventricular; Remodelings, Ventricular Cardiac; Remodeling, Ventricular Cardiac; Ventricular Cardiac Remodeling.
Where it fits in the MeSH classification
- Broader topics
- Pathological Conditions, Anatomical; Ventricular Function
Related concepts
- Heart Ventricles
- Myocardial Infarction
Research landscape
PubMed indexes 17,091 records tagged with the MeSH heading “Ventricular Remodeling” (counts retrieved 2026-10-29). 4,790 of them (28.0%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 7,838 records.
Reviews account for 2,551 records (14.9%) and meta-analyses for 147. Randomized controlled trials number 677 (4.0%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 4,517 |
| 2010-2019 | 7,838 |
| 2020 onward | 4,790 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,551 | 14.9% |
| Meta-analyses | 147 | 0.9% |
| Randomized controlled trials | 677 | 4.0% |
Method: PubMed query "Ventricular Remodeling"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
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.
Left Ventricular Remodeling After Myocardial Infarction-Pathophysiology, Diagnostic Approach and Management During Cardiac Rehabilitation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Despite the improvement in prognosis in patients with acute myocardial infarction (AMI), a significant proportion of survivors still experience heart failure (HF)-related adverse outcomes.
- Closing excerpt
- Finally, we provide up-to-date recommendations for the follow-up and management of LVR in post-AMI patients enrolled in CR and outline future prospects on this topic.
- 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 (129 words)
Despite the improvement in prognosis in patients with acute myocardial infarction (AMI), a significant proportion of survivors still experience heart failure (HF)-related adverse outcomes. Adverse left ventricular remodeling (LVR), which refers to a progressive dilation of left ventricular (LV) end-diastolic and end-systolic volumes, usually accompanied by a deterioration in LV systolic function, occurs frequently and underlies most cases of HF development after AMI. In this review, we discuss the current definitions of post-AMI LVR, the most appropriate imaging modalities for its detection, and the pathophysiological mechanisms by which Cardiac Rehabilitation (CR) can improve LVR-including exercise interventions, cardiovascular risk factors control, and pharmacological therapy optimization. Finally, we provide up-to-date recommendations for the follow-up and management of LVR in post-AMI patients enrolled in CR and outline future prospects on this topic.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41303447 · DOI · PMC12652362
Macrophages in ventricular remodeling and heart failure: orchestrators of inflammation and repair [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Heart failure is a complex clinical syndrome caused by structural and/or functional cardiac abnormalities.
- Closing excerpt
- Together, these insights provide a framework for understanding macrophage-mediated remodeling and for guiding precision immunotherapies in heart failure.
- 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 (163 words)
Heart failure is a complex clinical syndrome caused by structural and/or functional cardiac abnormalities. Ventricular remodeling contributes to its progression. Cardiac macrophages regulate inflammation, fibrosis, and tissue repair that drive this process. In this Review, we describe the origins and phenotypic diversity of cardiac macrophages, including both resident and monocyte-derived subsets. In the left ventricle, macrophages respond to ischemia, pressure overload, and metabolic stress. In the right ventricle, they display distinct immune features under pulmonary hypertension and other stress conditions. We further discuss the interactions between macrophages and other cardiac cell types, such as fibroblasts, cardiomyocytes, endothelial cells, and lymphocytes. These interactions shape the immune environment and structural integrity of the myocardium. We also highlight recent advances in single-cell and spatial technologies that reveal chamber-specific macrophage signatures. Finally, we summarize emerging therapeutic strategies targeting macrophages, including pharmacological agents, engineered cell therapies, and nanoparticle-based delivery systems. Together, these insights provide a framework for understanding macrophage-mediated remodeling and for guiding precision immunotherapies in heart failure.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41346626 · DOI · PMC12672248
A cross-study transcriptional patient map of heart failure defines conserved multicellular coordination in cardiac remodeling [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Impaired cardiac function in heart failure (HF) involves tissue remodeling through multicellular coordination.
- Closing excerpt
- This integrative analysis across studies establishes a public reference for the exploration of multicellular coordination in HF.
- 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 (147 words)
Impaired cardiac function in heart failure (HF) involves tissue remodeling through multicellular coordination. Although individual bulk and single-nucleus transcriptomics studies have offered insights, they have not been integrated to study conserved tissue-wide responses, limiting understanding of multicellular processes in cardiac remodeling necessary for therapeutic translation. Here, we integrate 25 studies of bulk and single-nucleus transcriptomics, spanning 1524 individuals, to define consensus multicellular programs associated with HF. These programs reveal conserved fibrotic, inflammatory, metabolic, and hypertrophic processes, with fibroblast activity consistently predicting cardiomyocyte stress. Our integration revealed that multicellular programs in HF are largely independent of tissue composition, and that fibroblast activation reflects a broad phenotypic shift rather than solely the emergence of discrete subtypes. Projecting external datasets onto these programs showed that clinical recovery aligns with reversion of disease-associated programs. This integrative analysis across studies establishes a public reference for the exploration of multicellular coordination in HF.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41173856 · DOI · PMC12579254
CCL5 promotes angiotensin II-induced cardiac remodeling through regulation of platelet-driven M2 macrophage polarization [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Rationale: Sustained hypertension induces adverse cardiac remodeling.
- Closing excerpt
- These findings support CCL5 inhibition as a promising strategy against inflammation and cardiac damage.
- 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 (300 words)
Rationale: Sustained hypertension induces adverse cardiac remodeling. Platelet activation is instrumental in exacerbating inflammation by engaging with macrophages. C-C chemokine motif ligand 5 (CCL5) is contained within platelet α-granules, and released following platelet activation. This work delineated the specific contributions of CCL5 to platelet function, platelet-induced macrophage polarization, and hypertensive cardiac remodeling. Methods: CCL5 knockout (KO) mice infused with Angiotensin II (Ang II) were used to identify the role of CCL5 in vivo. CCL5 absence on platelet activation were evaluated on washed platelets. Two distinct models of platelet depletion and reconstitution were utilized to investigate the impact of platelets lacking CCL5. An in vitro co-culture system was established to explore the roles of CCL5-mediated platelet activation in M2 macrophage polarization. Results: CCL5 KO attenuated the adverse cardiac effects induced by Ang II, including fibrosis, hypertrophy, and functional impairment, accompanied by reduced platelet activation and M2 macrophage polarization in cardiac tissue. Platelet inhibitor administration and platelet depletion/reconstitution experiments revealed that the suppression of platelet activation by CCL5 KO contributed to the amelioration of Ang II-promoted cardiac M2 macrophage polarization and cardiac remodeling. CCL5 KO markedly suppressed the activation of TGF-β1 and NF-κB signaling, an effect observed both in cardiac tissue from Ang II-infused mice and in platelets following ADP stimulation in vitro. In in vitro co-culture systems, rmTGF-β1 reversed CCL5 KO platelet-impaired M2 macrophage polarization. NF-κB inhibition abolished recombinant CCL5 (rmCCL5)-induced platelet activation, while blocking antibodies against CCR1 and CCR3 inhibited rmCCL5-induced NF-κB signaling and platelet activation. Conclusions: These findings underscore the detrimental role of CCL5-mediated platelet activation in promoting M2 macrophage polarization during hypertensive cardiac remodeling and elucidate the molecular mechanism that CCL5 facilitates platelet-derived TGF-β1 signaling by promoting NF-κB activation via CCR1 and CCR3 receptors. These findings support CCL5 inhibition as a promising strategy against inflammation and cardiac damage.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41346713 · DOI · PMC12674933
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 Mechanisms of physiological and pathological cardiac hypertrophy [5]
- Research article Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities [6]
- Research article Cardiac monocytes and macrophages after myocardial infarction [7]
- Research article T1 Mapping: Basic Techniques and Clinical Applications [8]
- Research article Therapeutic approaches for cardiac regeneration and repair [9]
- Research article Metabolic Coordination of Physiological and Pathological Cardiac Remodeling [10]
References
- Marcos-Garcés V, Bertolín-Boronat C, Merenciano-González H, Martínez Mas ML, Climent Alberola JI, López-Bueno L, et al.. Left Ventricular Remodeling After Myocardial Infarction-Pathophysiology, Diagnostic Approach and Management During Cardiac Rehabilitation. . 2025. PMID 41303447 · DOI · PMC12652362
- Feng H, Hu W, Liu Y, Xu X, Zhou P, Qu C, et al.. Macrophages in ventricular remodeling and heart failure: orchestrators of inflammation and repair. . 2025. PMID 41346626 · DOI · PMC12672248
- Lanzer JD, Ramirez Flores RO, Liñares Blanco J, Steier M, Rangrez AY, Frey N, et al.. A cross-study transcriptional patient map of heart failure defines conserved multicellular coordination in cardiac remodeling. . 2025. PMID 41173856 · DOI · PMC12579254
- Lv S, Zhou M, Li T, Zeng Z, Yan Z, Hou Y, et al.. CCL5 promotes angiotensin II-induced cardiac remodeling through regulation of platelet-driven M2 macrophage polarization. . 2026. PMID 41346713 · DOI · PMC12674933
- Nakamura M, Sadoshima J. Mechanisms of physiological and pathological cardiac hypertrophy. Nat Rev Cardiol. 2018. PMID 29674714 · DOI
- Ong SB, Hernández-Reséndiz S, Crespo-Avilan GE, Mukhametshina RT, Kwek XY, Cabrera-Fuentes HA, et al.. Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities. Pharmacol Ther. 2018. PMID 29330085 · DOI · PMC5981007
- Peet C, Ivetic A, Bromage DI, Shah AM. Cardiac monocytes and macrophages after myocardial infarction. Cardiovasc Res. 2020. PMID 31841135 · DOI · PMC7177720
- Taylor AJ, Salerno M, Dharmakumar R, Jerosch-Herold M. T1 Mapping: Basic Techniques and Clinical Applications. JACC Cardiovasc Imaging. 2016. PMID 26762877 · DOI
- Hashimoto H, Olson EN, Bassel-Duby R. Therapeutic approaches for cardiac regeneration and repair. Nat Rev Cardiol. 2018. PMID 29872165 · DOI · PMC6241533
- Gibb AA, Hill BG. Metabolic Coordination of Physiological and Pathological Cardiac Remodeling. Circ Res. 2018. PMID 29929976 · DOI · PMC6023588
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 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
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.