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Cutting-Edge Advances in Cardiac Development, Anatomy, and Regeneration
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Cutting-Edge Advances in Cardiac Development, Anatomy, and Regeneration

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425). This special issue belongs to the section "Cardiac Development and Regeneration".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 5199

Editor

Prof. Dr. Diego Franco Jaime

E-Mail Website
Guest Editor
Departamento de Biología Experimental, Universidad de Jaen, 23071 Jaen, Spain
Interests: cardiovascular development; transcriptional and post-transcriptional regulation; cardiac arrhythmias; organoids and cardioids
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The overarching aim of ICDAR 2025 is to advance understanding and innovation in cardiovascular development, anatomy, and regeneration, thereby contributing to the broader progress of cardiovascular science and medicine. This Special Issue will feature selected papers from the International Cardiovascular Development Anatomy and Regeneration Meeting (ICDAR 2025) and will highlight research across several key domains of multidisciplinary expertise: developmental mechanisms of the heart and vasculature, structural and functional cardiovascular anatomy, regenerative strategies and therapies, and translational applications in cardiovascular health and disease.

This Special Issue is in collaboration with the International Cardiovascular Development Anatomy and Regeneration Meeting (ICDAR 2025). It will provide an opportunity to showcase state-of-the-art research, review recent advances, and offer a strategic outlook on future directions in cardiovascular development and regenerative medicine. All speakers and poster presenters participating in this meeting are invited to submit a manuscript for consideration in this Special Issue. We also warmly welcome submissions from scholars who did not attend the meeting but are engaged in related areas of research.

Prof. Dr. Diego Franco Jaime
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Cardiovascular Development and Disease is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cardiac structure
  • congenital heart diseases
  • cardiovascular progenitors
  • regulatory mechanisms of cardiac development
  • cardiovascular epigenetics and differentiation
  • arrhythmias and the cardiac conduction system
  • cardiac valves
  • vascular development
  • cardiac repair and regeneration
  • cardiac engineering and organoids

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Published Papers (4 papers)

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Research

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17 pages, 7050 KB  
Article
RNA-Binding Protein Trim71 Controls Epicardial Cell Migration
by Juan Manuel Castillo-Casas, Carlos García-Padilla, Rita Carmona, Estefanía Lozano-Velasco and Diego Franco
J. Cardiovasc. Dev. Dis. 2026, 13(6), 237; https://doi.org/10.3390/jcdd13060237 - 31 May 2026
Viewed by 316
Abstract
The epicardium is an embryonic tissue layer essential for heart morphogenesis, providing progenitor cells and regulatory signals that support myocardial growth and coronary vessel formation. Epicardial cells arise from the proepicardium (PE) and spread over the myocardium to form the embryonic epicardium (EE), [...] Read more.
The epicardium is an embryonic tissue layer essential for heart morphogenesis, providing progenitor cells and regulatory signals that support myocardial growth and coronary vessel formation. Epicardial cells arise from the proepicardium (PE) and spread over the myocardium to form the embryonic epicardium (EE), a transition that requires tight coordination between proliferation, migration, and lineage priming. However, the molecular mechanisms controlling this developmental timing remain incompletely understood. Here, we identify Trim71 as a key regulator of epicardial cell behaviour during the PE-to-EE transition. Trim71 is enriched in the PE and subsequently downregulated as cells acquire migratory competence. Functional analyses show that loss of Trim71 function decreases proliferation while promoting migration, as well as inducing the expression of epicardial commitment markers, suggesting that Trim71 is a controller of a progenitor-like state. We further demonstrate that Trim71 is necessary for these processes through a reciprocal feedback loop with the microRNAs let-7c and miR-30c. Our findings establish Trim71 as a temporal gatekeeper that coordinates the balance between progenitor maintenance and migration during early epicardial development. This Trim71-miRNAs axis constitutes a novel post-transcriptional layer of regulation that ensures the correct timing of epicardium development during cardiogenesis. Full article
(This article belongs to the Special Issue Cutting-Edge Advances in Cardiac Development, Anatomy, and Regeneration)
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12 pages, 6022 KB  
Article
Inferior Left Atrial Diverticulum Communicating with the Right Atrium or Inferior Vena Cava: Prevalence and CT Features
by Hae Jin Kim, Sung Goo Park, Sung-A Chang, Jinyoung Song, Ji Hyuk Yang, Sung Mok Kim and Yeon Hyeon Choe
J. Cardiovasc. Dev. Dis. 2026, 13(5), 215; https://doi.org/10.3390/jcdd13050215 - 17 May 2026
Cited by 1 | Viewed by 898
Abstract
Purpose: To evaluate the prevalence and cardiac CT features of inferior left atrial diverticula (ILAD) communicating with the right atrium (RA) or inferior vena cava (IVC), a novel type of interatrial communication. Materials and Methods: This retrospective study included 11,512 consecutive patients who [...] Read more.
Purpose: To evaluate the prevalence and cardiac CT features of inferior left atrial diverticula (ILAD) communicating with the right atrium (RA) or inferior vena cava (IVC), a novel type of interatrial communication. Materials and Methods: This retrospective study included 11,512 consecutive patients who underwent cardiac CT. CT features and prevalence of ILAD communicating with the RA or IVC were analyzed. Shunts were defined as anatomical defects between the two structures with or without visible contrast flow. In a subset of the patients we compared interatrial septal aneurysm (n = 20) and ILAD without shunt (n = 66), assessing the involvement of a wedge-like fatty space bordered by both atria, IVC and coronary sinus. Results: There were 33 patients (19 males and 14 females; aged 59.8 ± 11.2 years; age range, 18–87 years) with ILAD with shunts (ILADSs). The prevalence of ILADSs was 4.2% (33/783) among ILAD and 0.3% (33/11,512) among all patients. Maximal dimensions of ILAD were 17.6 ± 9.9 mm (range, 5.3–41.0 mm). Mean ostial diameters of ILAD and mean sizes of shunts were 6.2 ± 5.6 mm and 3.2 ± 2.9 mm, respectively. Shunts were larger than 5 mm in 6 patients (15.2%) and larger than 3 mm in 10 patients (30.3%). In 30 patients who underwent transthoracic echocardiography, ILADSs were not identified at echocardiography. CT showed involvement of the wedge-like fatty space for all ILAD and for no cases with interatrial septal aneurysm. Conclusions: Cardiac CT enables detection of incidental ILADSs unrecognized at echocardiography. Full article
(This article belongs to the Special Issue Cutting-Edge Advances in Cardiac Development, Anatomy, and Regeneration)
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Review

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17 pages, 1169 KB  
Review
ROS-Mediated Cardiomyocyte Proliferation and Myocardial Regeneration: Mechanisms and Targeted Strategies for Ischemic Heart Disease
by Mengqi Chen, Tingting Liu, Fangling Sun, Xin Tian, Wenrong Zheng, Zixin Zhu and Wen Wang
J. Cardiovasc. Dev. Dis. 2026, 13(3), 105; https://doi.org/10.3390/jcdd13030105 - 25 Feb 2026
Viewed by 1648
Abstract
Cardiovascular disease (CVD) persists as the leading cause of global mortality, with adult mammalian hearts exhibiting limited regenerative capacity. Although cardiomyocytes (CMs) can re-enter the cell cycle and undergo DNA synthesis in response to injury, they fail to complete mitosis and cytokinesis, resulting [...] Read more.
Cardiovascular disease (CVD) persists as the leading cause of global mortality, with adult mammalian hearts exhibiting limited regenerative capacity. Although cardiomyocytes (CMs) can re-enter the cell cycle and undergo DNA synthesis in response to injury, they fail to complete mitosis and cytokinesis, resulting in a functional blockade of productive proliferation following ischemic or aging-related injury. Reactive oxygen species (ROS) exhibit a context-dependent duality in cardiac regeneration: while maintaining redox homeostasis and supporting developmental signaling at physiological concentrations, pathological ROS accumulation exacerbates myocardial decline by inducing DNA damage response (DDR)-mediated cell cycle arrest at G2/M phase, along with structural and functional impairments. This review examines the mechanisms of ROS generation—from its cellular origins to its molecular drivers—in ischemic heart disease, and explores the modulation of regenerative signaling by oxidative stress. We further critically assess emerging therapeutic interventions targeting ROS-mediated myocardial regeneration. By delineating the functional roles of ROS in cardiac injury and repair, this review provides a mechanistic and translational framework for developing redox-based therapies aimed at promoting cardiomyocyte proliferation and myocardial regeneration after ischemic injury. Full article
(This article belongs to the Special Issue Cutting-Edge Advances in Cardiac Development, Anatomy, and Regeneration)
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36 pages, 1598 KB  
Review
Engineering Mitochondrial Biogenesis in iPSC-CMs: CRISPR-Guided Approaches for Advanced Cardiomyocyte Development
by Dhienda C. Shahannaz, Tadahisa Sugiura, Brandon E. Ferrell and Taizo Yoshida
J. Cardiovasc. Dev. Dis. 2026, 13(2), 77; https://doi.org/10.3390/jcdd13020077 - 3 Feb 2026
Cited by 7 | Viewed by 1650
Abstract
Human iPSC-derived cardiomyocytes (iPSC-CMs) exhibit fetal-like mitochondrial networks and limited oxidative metabolism, constraining their translational utility. The key bottleneck is mitochondrial immaturity, resulting from blunted PGC-1α–NRF1/2–TFAM axis activation and insufficient nuclear–mitochondrial coordination, rather than sarcomeric or electrophysiological immaturity alone. This review synthesizes [...] Read more.
Human iPSC-derived cardiomyocytes (iPSC-CMs) exhibit fetal-like mitochondrial networks and limited oxidative metabolism, constraining their translational utility. The key bottleneck is mitochondrial immaturity, resulting from blunted PGC-1α–NRF1/2–TFAM axis activation and insufficient nuclear–mitochondrial coordination, rather than sarcomeric or electrophysiological immaturity alone. This review synthesizes genome-guided interventions (CRISPRa and mtDNA editing) and complementary environmental strategies—including metabolic substrate switching, electromechanical stimulation, and extracellular vesicle (EV)-mediated mitochondrial transfer—to drive mitochondrial biogenesis and maturation in iPSC-CMs. We systematically reviewed studies (2005–2025) targeting (1) key regulators of mitochondrial biogenesis (PGC-1α, NRF1/2, TFAM), (2) CRISPR-based transcriptional activators/repressors and mtDNA editors (DdCBE, mitoTALENs), and (3) maturation approaches such as metabolic conditioning, electromechanical stimulation, 3D tissue culture, and EV-mediated mitochondrial transfer. CRISPRa-mediated activation of PGC-1α, NRF1, and GATA4, combined with mtDNA base editors, enhances mitochondrial mass and OXPHOS function, while integration with environmental maturation strategies further promotes adult-like phenotypes. Integrative approaches that combine genome-guided interventions (CRISPRa, mtDNA editing) with environmental maturation cues yield the most adult-like iPSC-CM phenotypes reported to date. CRISPR-guided mitochondrial biogenesis thus represents a frontier for producing metabolically competent, structurally mature iPSC-CMs for disease modeling and therapy. Remaining translational challenges include efficient mitochondrial delivery, metabolic homeostasis, and multi-omics validation. We propose standardized workflows to couple nuclear and mitochondrial editing with maturation strategies. Full article
(This article belongs to the Special Issue Cutting-Edge Advances in Cardiac Development, Anatomy, and Regeneration)
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