A neonatal leporine model of age-dependent natural heart regeneration after myocardial infarction

Wang, Shuangfeng; Hironaka, Camille E.; Mullis, Danielle M.; Lucian, Haley J.; Shin, Hye Sook; Tran, Nicholas A.; Thakore, Akshara D.; Anilkumar, Shreya; Wu, Matthew A.; Paulsen, Michael J.; Zhu, Yuanjia; Baker, Sam W.; Woo, Y. Joseph

doi:10.1016/j.jtcvs.2021.08.013

Cited by 7 publications

(4 citation statements)

References 32 publications

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“…The adult guinea pig (Cavia porcellus) responds to cardiac cryoinjury with scarring and functional impairment 51 and, to date, no neonatal heart injury studies have been carried out in guinea pigs. In a study published in 2022, heart regeneration capacity was investigated in neonatal European rabbits (Oryctolagus cuniculus) 52 . Infarcted rabbit hearts displayed reduced scarring, as well as improved functional recovery, following MI at P1 when compared with MI at P7, mirroring the results obtained in the neonatal mouse heart.…”

Section: [H2] Mammalsmentioning

confidence: 99%

Animal models to study cardiac regeneration

Weinberger

Riley

2023

Nat Rev Cardiol

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Permanent fibrosis and chronic deterioration of heart function in human patientsfollowing myocardial infarction present a major healthcare burden worldwide. In contrast to the restricted potential for cellular and functional regeneration of the adult mammalian heart, a robust capacity for cardiac regeneration is seen during the during the neonatal period in mammals as well as in the adults of many fish and amphibian species. However, we lack a complete understanding as to why cardiac regeneration takes place more efficiently in some species than in others. The capacity of the heart to regenerate following injury is controlled by a complex network of cellular and molecular mechanisms that form a regulatory landscape, either permitting or restricting regeneration. In this Review, we provide an overview of the diverse array of vertebrates that have been studied for their cardiac regenerative potential and discuss differential heart regeneration outcomes in closely related species. Additionally, we summarize current knowledge about the core mechanisms that regulate cardiac regeneration across vertebrate species. [H1] IntroductionCardiovascular disease continues to be one of the major causes of death worldwide 1 .Although the survival rate for myocardial infarction (MI) -the death of heart muscle tissue due to a lack of oxygen caused by the disruption of coronary blood flow 2 -has been steadily

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Section: [H2] Mammalsmentioning

confidence: 99%

Animal models to study cardiac regeneration

Weinberger

Riley

2023

Nat Rev Cardiol

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“…Neonatal mice which undergo apical resection or ligation of the left coronary artery on postnatal day 1 (P1) exhibit complete cardiac regeneration with proliferation of cardiomyocytes and minimal fibrosis, although this ability is lost if injury occurs after postnatal day 7 (P7) 15 , 24 . An apparently conserved neonatal cardiac regeneration response has also been identified in other mammalian species as well, including rats 25 , rabbits 26 , and pigs 27 , 28 . In humans, cardiomyocyte turnover and renewal has been detected in the postnatal human heart 23 , 29 , 30 .…”

Section: Mammalian Response To Cardiac Injurymentioning

confidence: 93%

Structural, angiogenic, and immune responses influencing myocardial regeneration: a glimpse into the crucible

Baccouche,

Elde,

Wang

et al. 2024

npj Regen Med

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Complete cardiac regeneration remains an elusive therapeutic goal. Although much attention has been focused on cardiomyocyte proliferation, especially in neonatal mammals, recent investigations have unearthed mechanisms by which non-cardiomyocytes, such as endothelial cells, fibroblasts, macrophages, and other immune cells, play critical roles in modulating the regenerative capacity of the injured heart. The degree to which each of these cell types influence cardiac regeneration, however, remains incompletely understood. This review highlights the roles of these non-cardiomyocytes and their respective contributions to cardiac regeneration, with emphasis on natural heart regeneration after cardiac injury during the neonatal period.

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“…In most mammals, cardiomyocytes permanently exit the cell cycle and become polyploid due to failure in either cytokinesis or karyokinesis in the perinatal window [19][20][21][22][23]. This coincides with the closure of cardiac regenerative period in mice, rats, rabbits and pigs [24][25][26][27][28]. Indeed, it has been shown that stimulation of cardiomyocyte proliferation enhances cardiac regeneration and reverse heart failure [29,30].…”

Section: Divergence In Ontogenymentioning

confidence: 99%