PDF(Pubmed)
Abstract：
UNASSIGNED: Cardiovascular diseases have been the leading cause of death globally for decades. Pharmacological advances targeting the sympathetic nervous system, renin-angiotensin-aldosterone system, and fibrosis slow the progression of diverse cardiovascular diseases. However, ongoing cardiomyocyte loss is inevitable in divergent cardiovascular diseases, eventually leading to heart failure as the end stage. In this review, we focused on the key biomedical findings and underlying principles of cardiomyocyte regeneration.
UNASSIGNED: Literature regarding the key findings in cardiomyocyte regeneration research, including controversies on the origins of newly formed cardiomyocytes, potential barriers and strategies to heart regeneration, and the key animals, models, and methods applied in the study of heart regeneration, were broadly researched using the PubMed and Web of Science databases.
UNASSIGNED: In the mammalian heart, cardiomyocytes proliferate during the embryonic and early postnatal stages, while the capability of proliferation disappears in the adult stage. An increasing amount of evidence suggests that cardiomyocytes self-renew at a very limited level and that most newly formed cardiomyocytes originate from pre-existing cardiomyocytes and not cardiac progenitor cells (CPCs). Several potential barriers to heart regeneration have been addressed, including metabolic switch, a large increase in multinucleated and polyploid cardiomyocytes, and alteration in the epigenome and transcriptome. In addition, immune system evolution is also associated with the loss of regenerative capacity. However, the activation of resident cardiomyocytes, somatic cell reprogramming, and direct reprogramming, in addition to the promotion of neovascularization and immune modulation, constitute the new insights into those strategies that can boost cardiac regeneration.
UNASSIGNED: Heart regeneration is one of the most popular fields in cardiovascular research and represents a promising avenue of therapeutics for mending a broken heart. Despite the controversies and challenges, a clearer picture of adult mammalian cardiac regeneration is emerging.
UNASSIGNED: Literature regarding the key findings in cardiomyocyte regeneration research, including controversies on the origins of newly formed cardiomyocytes, potential barriers and strategies to heart regeneration, and the key animals, models, and methods applied in the study of heart regeneration, were broadly researched using the PubMed and Web of Science databases.
UNASSIGNED: In the mammalian heart, cardiomyocytes proliferate during the embryonic and early postnatal stages, while the capability of proliferation disappears in the adult stage. An increasing amount of evidence suggests that cardiomyocytes self-renew at a very limited level and that most newly formed cardiomyocytes originate from pre-existing cardiomyocytes and not cardiac progenitor cells (CPCs). Several potential barriers to heart regeneration have been addressed, including metabolic switch, a large increase in multinucleated and polyploid cardiomyocytes, and alteration in the epigenome and transcriptome. In addition, immune system evolution is also associated with the loss of regenerative capacity. However, the activation of resident cardiomyocytes, somatic cell reprogramming, and direct reprogramming, in addition to the promotion of neovascularization and immune modulation, constitute the new insights into those strategies that can boost cardiac regeneration.
UNASSIGNED: Heart regeneration is one of the most popular fields in cardiovascular research and represents a promising avenue of therapeutics for mending a broken heart. Despite the controversies and challenges, a clearer picture of adult mammalian cardiac regeneration is emerging.
摘要：
未经证实：几十年来，心血管疾病一直是全球死亡的主要原因。针对交感神经系统的药理学进展，肾素-血管紧张素-醛固酮系统，和纤维化减缓各种心血管疾病的进展。然而,在不同的心血管疾病中，持续的心肌细胞损失是不可避免的，最终导致心力衰竭为终点。在这次审查中,我们重点研究了心肌细胞再生的关键生物医学发现和基本原理.
未经证实：关于心肌细胞再生研究的主要发现的文献，包括关于新形成的心肌细胞起源的争议，心脏再生的潜在障碍和策略，和关键的动物，模型，以及在心脏再生研究中应用的方法，使用PubMed和WebofScience数据库进行了广泛的研究。
未经证实：在哺乳动物心脏中，心肌细胞在胚胎和出生后早期阶段增殖，而增殖能力在成年阶段消失。越来越多的证据表明，心肌细胞在非常有限的水平上自我更新，并且大多数新形成的心肌细胞起源于预先存在的心肌细胞，而不是心脏祖细胞（CPC）。已经解决了心脏再生的几个潜在障碍，包括代谢开关，多核和多倍体心肌细胞大量增加，以及表观基因组和转录组的改变。此外,免疫系统的进化也与再生能力的丧失有关。然而,驻留心肌细胞的激活，体细胞重编程，和直接重新编程，除了促进新生血管形成和免疫调节，构成了对那些可以促进心脏再生的策略的新见解。
UNASSIGNED：心脏再生是心血管研究中最受欢迎的领域之一，代表了修复破碎心脏的有希望的治疗途径。尽管存在争议和挑战，成年哺乳动物心脏再生的更清晰的图像正在出现。
未经证实：关于心肌细胞再生研究的主要发现的文献，包括关于新形成的心肌细胞起源的争议，心脏再生的潜在障碍和策略，和关键的动物，模型，以及在心脏再生研究中应用的方法，使用PubMed和WebofScience数据库进行了广泛的研究。
未经证实：在哺乳动物心脏中，心肌细胞在胚胎和出生后早期阶段增殖，而增殖能力在成年阶段消失。越来越多的证据表明，心肌细胞在非常有限的水平上自我更新，并且大多数新形成的心肌细胞起源于预先存在的心肌细胞，而不是心脏祖细胞（CPC）。已经解决了心脏再生的几个潜在障碍，包括代谢开关，多核和多倍体心肌细胞大量增加，以及表观基因组和转录组的改变。此外,免疫系统的进化也与再生能力的丧失有关。然而,驻留心肌细胞的激活，体细胞重编程，和直接重新编程，除了促进新生血管形成和免疫调节，构成了对那些可以促进心脏再生的策略的新见解。
UNASSIGNED：心脏再生是心血管研究中最受欢迎的领域之一，代表了修复破碎心脏的有希望的治疗途径。尽管存在争议和挑战，成年哺乳动物心脏再生的更清晰的图像正在出现。
