Nature cardiovascular research最新文献_第9页

Macrophages enable heart-on-a-chip longevity 巨噬细胞让芯片心脏长寿

IF 9.4

Nature cardiovascular research Pub Date : 2024-07-03 DOI: 10.1038/s44161-024-00519-8

Michelle Korda

引用次数: 0

Trained brain–heart biofeedback lowers heart rate 经过训练的脑-心生物反馈可降低心率

IF 9.4

Nature cardiovascular research Pub Date : 2024-07-03 DOI: 10.1038/s44161-024-00518-9

Gerburg Schwaerzer

引用次数: 0

Autologous PSC-CMs show long-term engraftment after infarction in non-human primates 非人灵长类动物脑梗塞后自体 PSC-CMs 显示出长期移植效果

IF 9.4

Nature cardiovascular research Pub Date : 2024-07-02 DOI: 10.1038/s44161-024-00514-z

Andrea Tavosanis

引用次数: 0

Author Correction: Accelerated biological aging elevates the risk of cardiometabolic multimorbidity and mortality 作者更正：生物老化加速会增加心脏代谢多病和死亡风险

IF 9.4

Nature cardiovascular research Pub Date : 2024-06-27 DOI: 10.1038/s44161-024-00515-y

Meijie Jiang, Sifan Tian, Shuzhen Liu, Yuting Wang, Xinbiao Guo, Tao Huang, Xihong Lin, Daniel W. Belsky, Andrea A. Baccarelli, Xu Gao

引用次数: 0

A renaissance of cerebral cavernous malformation proteins in vascular physiology 脑海绵畸形蛋白在血管生理学中的复兴

IF 9.4

Nature cardiovascular research Pub Date : 2024-06-27 DOI: 10.1038/s44161-024-00504-1

Salim Abdelilah-Seyfried, Hanjoong Jo

引用次数: 0

Cellular senescence is required for cardiac regeneration 心脏再生需要细胞衰老

IF 9.4

Nature cardiovascular research Pub Date : 2024-06-26 DOI: 10.1038/s44161-024-00494-0

引用次数: 0

Assessing the arrhythmogenic propensity of fibrotic substrate using digital twins to inform a mechanisms-based atrial fibrillation ablation strategy 利用数字双胞胎评估纤维基质的致心律失常倾向，为基于机制的心房颤动消融策略提供依据

IF 9.4

Nature cardiovascular research Pub Date : 2024-06-18 DOI: 10.1038/s44161-024-00489-x

Kensuke Sakata, Ryan P. Bradley, Adityo Prakosa, Carolyna A. P. Yamamoto, Syed Yusuf Ali, Shane Loeffler, Brock M. Tice, Patrick M. Boyle, Eugene G. Kholmovski, Ritu Yadav, Sunil Kumar Sinha, Joseph E. Marine, Hugh Calkins, David D. Spragg, Natalia A. Trayanova

{"title":"Assessing the arrhythmogenic propensity of fibrotic substrate using digital twins to inform a mechanisms-based atrial fibrillation ablation strategy","authors":"Kensuke Sakata, Ryan P. Bradley, Adityo Prakosa, Carolyna A. P. Yamamoto, Syed Yusuf Ali, Shane Loeffler, Brock M. Tice, Patrick M. Boyle, Eugene G. Kholmovski, Ritu Yadav, Sunil Kumar Sinha, Joseph E. Marine, Hugh Calkins, David D. Spragg, Natalia A. Trayanova","doi":"10.1038/s44161-024-00489-x","DOIUrl":"10.1038/s44161-024-00489-x","url":null,"abstract":"Atrial fibrillation (AF), the most common heart rhythm disorder, may cause stroke and heart failure. For patients with persistent AF with fibrosis proliferation, the standard AF treatment—pulmonary vein isolation—has poor outcomes, necessitating redo procedures, owing to insufficient understanding of what constitutes good targets in fibrotic substrates. Here we present a prospective clinical and personalized digital twin study that characterizes the arrhythmogenic properties of persistent AF substrates and uncovers locations possessing rotor-attracting capabilities. Among these, a portion needs to be ablated to render the substrate not inducible for rotors, but the rest (37%) lose rotor-attracting capabilities when another location is ablated. Leveraging digital twin mechanistic insights, we suggest ablation targets that eliminate arrhythmia propensity with minimum lesions while also minimizing the risk of iatrogenic tachycardia and AF recurrence. Our findings provide further evidence regarding the appropriate substrate ablation targets in persistent AF, opening the door for effective strategies to mitigate patients’ AF burden. Sakata et al. performed a prospective personalized mechanistic computational (digital twin) study focused on characterizing the arrhythmogenic properties of the atrial fibrotic substrate in patients with persistent atrial fibrillation, and they introduce here a novel mechanism-oriented strategy for optimal ablation.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 7","pages":"857-868"},"PeriodicalIF":9.4,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44161-024-00489-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141639676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Distinct biological signature and modifiable risk factors underlie the comorbidity between major depressive disorder and cardiovascular disease 重度抑郁障碍与心血管疾病之间的共病现象是由不同的生物特征和可改变的风险因素造成的

Nature cardiovascular research Pub Date : 2024-06-17 DOI: 10.1038/s44161-024-00488-y

Jacob Bergstedt, Joëlle A. Pasman, Ziyan Ma, Arvid Harder, Shuyang Yao, Nadine Parker, Jorien L. Treur, Dirk J. A. Smit, Oleksandr Frei, Alexey A. Shadrin, Joeri J. Meijsen, Qing Shen, Sara Hägg, Per Tornvall, Alfonso Buil, Thomas Werge, Jens Hjerling-Leffler, Thomas D. Als, Anders D. Børglum, Cathryn M. Lewis, Andrew M. McIntosh, Unnur A. Valdimarsdóttir, Ole A. Andreassen, Patrick F. Sullivan, Yi Lu, Fang Fang

{"title":"Distinct biological signature and modifiable risk factors underlie the comorbidity between major depressive disorder and cardiovascular disease","authors":"Jacob Bergstedt, Joëlle A. Pasman, Ziyan Ma, Arvid Harder, Shuyang Yao, Nadine Parker, Jorien L. Treur, Dirk J. A. Smit, Oleksandr Frei, Alexey A. Shadrin, Joeri J. Meijsen, Qing Shen, Sara Hägg, Per Tornvall, Alfonso Buil, Thomas Werge, Jens Hjerling-Leffler, Thomas D. Als, Anders D. Børglum, Cathryn M. Lewis, Andrew M. McIntosh, Unnur A. Valdimarsdóttir, Ole A. Andreassen, Patrick F. Sullivan, Yi Lu, Fang Fang","doi":"10.1038/s44161-024-00488-y","DOIUrl":"10.1038/s44161-024-00488-y","url":null,"abstract":"Major depressive disorder (MDD) and cardiovascular disease (CVD) are often comorbid, resulting in excess morbidity and mortality. Here we show that CVDs share most of their genetic risk factors with MDD. Multivariate genome-wide association analysis of shared genetic liability between MDD and atherosclerotic CVD revealed seven loci and distinct patterns of tissue and brain cell-type enrichments, suggesting the involvement of the thalamus. Part of the genetic overlap was explained by shared inflammatory, metabolic and psychosocial or lifestyle risk factors. Our data indicated causal effects of genetic liability to MDD on CVD risk, but not from most CVDs to MDD, and showed that the causal effects were partly explained by metabolic and psychosocial or lifestyle factors. The distinct signature of MDD–atherosclerotic CVD comorbidity suggests an immunometabolic subtype of MDD that is more strongly associated with CVD than overall MDD. In summary, we identified biological mechanisms underlying MDD–CVD comorbidity and modifiable risk factors for prevention of CVD in individuals with MDD. Bergstedt et al. show that the effects of genetic liability to major depressive disorder can cause an increase in cardiovascular risk and that metabolic, psychological and lifestyle factors are partly responsible for this association.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 6","pages":"754-769"},"PeriodicalIF":0.0,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44161-024-00488-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141425148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Redefining common and rare HTRA1 variants as risk factors for polyvascular disease 将常见和罕见的 HTRA1 变异重新定义为多血管疾病的风险因素

Nature cardiovascular research Pub Date : 2024-06-14 DOI: 10.1038/s44161-024-00492-2

Stéphanie Debette, Masafumi Ihara

引用次数: 0

Egr1 regulates regenerative senescence and cardiac repair Egr1 调控再生衰老和心脏修复

IF 9.4

Nature cardiovascular research Pub Date : 2024-06-14 DOI: 10.1038/s44161-024-00493-1

Lingling Zhang, Jacob Elkahal, Tianzhen Wang, Racheli Rimmer, Alexander Genzelinakh, Elad Bassat, Jingkui Wang, Dahlia Perez, David Kain, Daria Lendengolts, Roni Winkler, Hanna Bueno-levy, Kfir Baruch Umansky, David Mishaly, Avraham Shakked, Shoval Miyara, Avital Sarusi-Portuguez, Naomi Goldfinger, Amir Prior, David Morgenstern, Yishai Levin, Yoseph Addadi, Baoguo Li, Varda Rotter, Uriel Katz, Elly M. Tanaka, Valery Krizhanovsky, Rachel Sarig, Eldad Tzahor

{"title":"Egr1 regulates regenerative senescence and cardiac repair","authors":"Lingling Zhang, Jacob Elkahal, Tianzhen Wang, Racheli Rimmer, Alexander Genzelinakh, Elad Bassat, Jingkui Wang, Dahlia Perez, David Kain, Daria Lendengolts, Roni Winkler, Hanna Bueno-levy, Kfir Baruch Umansky, David Mishaly, Avraham Shakked, Shoval Miyara, Avital Sarusi-Portuguez, Naomi Goldfinger, Amir Prior, David Morgenstern, Yishai Levin, Yoseph Addadi, Baoguo Li, Varda Rotter, Uriel Katz, Elly M. Tanaka, Valery Krizhanovsky, Rachel Sarig, Eldad Tzahor","doi":"10.1038/s44161-024-00493-1","DOIUrl":"10.1038/s44161-024-00493-1","url":null,"abstract":"Senescence plays a key role in various physiological and pathological processes. We reported that injury-induced transient senescence correlates with heart regeneration, yet the multi-omics profile and molecular underpinnings of regenerative senescence remain obscure. Using proteomics and single-cell RNA sequencing, here we report the regenerative senescence multi-omic signature in the adult mouse heart and establish its role in neonatal heart regeneration and agrin-mediated cardiac repair in adult mice. We identified early growth response protein 1 (Egr1) as a regulator of regenerative senescence in both models. In the neonatal heart, Egr1 facilitates angiogenesis and cardiomyocyte proliferation. In adult hearts, agrin-induced senescence and repair require Egr1, activated by the integrin–FAK–ERK–Akt1 axis in cardiac fibroblasts. We also identified cathepsins as injury-induced senescence-associated secretory phenotype components that promote extracellular matrix degradation and potentially assist in reducing fibrosis. Altogether, we uncovered the molecular signature and functional benefits of regenerative senescence during heart regeneration, with Egr1 orchestrating the process. Zhang et al. show that Egr1 regulates transient senescence during neonatal heart regeneration and upon agrin-mediated cardiac repair in adult mice, acting downstream of the integrin–FAK–ERK–Akt1 axis in cardiac fibroblasts.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 8","pages":"915-932"},"PeriodicalIF":9.4,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141344256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0