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Enhanced Trained Immunity in Peripheral Monocytes in Unstable Angina With Elevated High-Sensitivity C-Reactive Protein 不稳定心绞痛患者外周血单核细胞训练免疫增强伴高敏c反应蛋白升高
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-06-24 DOI: 10.1016/j.jacbts.2025.04.014
Jiyu Zhang PhD , Fen Yang MD , Yuhan Liao MD , Xinyi Xia MS , Miao Yu MD, PhD , Desheng Hu MD, PhD , Weimin Wang MD, PhD , Li Zhang MD, PhD , Chaolong Wang PhD , Huirong Liu MD, PhD , Chen Chen MD, PhD , Qing K. Wang PhD , Zhilei Shan PhD , Peter Libby MD, PhD , Xiang Cheng MD, PhD
{"title":"Enhanced Trained Immunity in Peripheral Monocytes in Unstable Angina With Elevated High-Sensitivity C-Reactive Protein","authors":"Jiyu Zhang PhD ,&nbsp;Fen Yang MD ,&nbsp;Yuhan Liao MD ,&nbsp;Xinyi Xia MS ,&nbsp;Miao Yu MD, PhD ,&nbsp;Desheng Hu MD, PhD ,&nbsp;Weimin Wang MD, PhD ,&nbsp;Li Zhang MD, PhD ,&nbsp;Chaolong Wang PhD ,&nbsp;Huirong Liu MD, PhD ,&nbsp;Chen Chen MD, PhD ,&nbsp;Qing K. Wang PhD ,&nbsp;Zhilei Shan PhD ,&nbsp;Peter Libby MD, PhD ,&nbsp;Xiang Cheng MD, PhD","doi":"10.1016/j.jacbts.2025.04.014","DOIUrl":"10.1016/j.jacbts.2025.04.014","url":null,"abstract":"<div><div>Despite effective secondary prevention for coronary heart diseases, recurrent events remain high. Elevated high-sensitivity C-reactive protein (hsCRP) indicates increased inflammation risk. This study aimed to investigate the trained immunity of circulating monocytes in unstable angina (UA) patients with elevated hsCRP. We analyzed CD14<sup>+</sup> monocytes from UA patients, comparing high-risk (hsCRP ≥3 mg/L) and low-risk (hsCRP &lt;1 mg/L) groups. We assessed cytokine production and conducted metabolic, transcriptional, and epigenetic profiling. Patients with elevated hsCRP exhibited enhanced proinflammatory responses, glycolytic activity, and altered immune profiles, indicating sustained monocyte trained immunity, which contributes to residual inflammation risk in cardiovascular disease.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 7","pages":"Article 101300"},"PeriodicalIF":8.4,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144470606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
High Maternal Glycine Levels Increase the Risk of Developing Atrial Septal Defect in the Offspring 母体甘氨酸水平高会增加子代房间隔缺损的风险
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-06-24 DOI: 10.1016/j.jacbts.2025.05.006
Ya-Nan Qiao PhD , Wei-Cheng Chen PhD , Yu-Ling Chen MD , Jie Xiang BS , Yu-Fan Ke BS , Li Cao PhD , Lei Li PhD , Jing Cao PhD , Rui Zhao PhD , Jian-Yuan Zhao PhD
{"title":"High Maternal Glycine Levels Increase the Risk of Developing Atrial Septal Defect in the Offspring","authors":"Ya-Nan Qiao PhD ,&nbsp;Wei-Cheng Chen PhD ,&nbsp;Yu-Ling Chen MD ,&nbsp;Jie Xiang BS ,&nbsp;Yu-Fan Ke BS ,&nbsp;Li Cao PhD ,&nbsp;Lei Li PhD ,&nbsp;Jing Cao PhD ,&nbsp;Rui Zhao PhD ,&nbsp;Jian-Yuan Zhao PhD","doi":"10.1016/j.jacbts.2025.05.006","DOIUrl":"10.1016/j.jacbts.2025.05.006","url":null,"abstract":"<div><div>Amino acid imbalance is linked to increased congenital heart disease risk. Here, we found women carrying rs2545801 C/C genotypes exhibited increased glycine levels and increased risk for atrial septal defects (ASDs) in their offspring. Elevated maternal glycine levels during the first trimester were correlated with a higher ASD risk in the offspring. Additionally, feeding pregnant mice with high-glycine chow increased ASD risk in their offspring. Mechanistically, elevated maternal glycine led to increased lysine-glycylation of lysine-688 within the TEK receptor tyrosine kinase and inhibited TEK-PI3K-AKT/FOXO1 signaling in cardiac endothelial cells. These findings indicate that lysine-glycylation exerts teratogenic effects and may be a target for ASD intervention.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 7","pages":"Article 101311"},"PeriodicalIF":8.4,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144365071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cardiac Injury Regulates Neuroinflammation Through Extracellular Vesicle–Mediated Heart-Brain Crosstalk 心脏损伤通过细胞外囊泡介导的心脑串扰调节神经炎症
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-06-23 DOI: 10.1016/j.jacbts.2025.05.002
Qingxuan Li BS , Ramzi H. Hamdalla MS , Neha Dhyani PhD , Lijun Sun BS , Lie Gao MD, PhD , Tara L. Rudebush BS , Irving H. Zucker PhD , Changhai Tian PhD
{"title":"Cardiac Injury Regulates Neuroinflammation Through Extracellular Vesicle–Mediated Heart-Brain Crosstalk","authors":"Qingxuan Li BS ,&nbsp;Ramzi H. Hamdalla MS ,&nbsp;Neha Dhyani PhD ,&nbsp;Lijun Sun BS ,&nbsp;Lie Gao MD, PhD ,&nbsp;Tara L. Rudebush BS ,&nbsp;Irving H. Zucker PhD ,&nbsp;Changhai Tian PhD","doi":"10.1016/j.jacbts.2025.05.002","DOIUrl":"10.1016/j.jacbts.2025.05.002","url":null,"abstract":"<div><div>Cognitive impairment is common in heart failure patients, contributing to morbidity and mortality. This impairment may be linked to neuroinflammation in heart failure. However, the primacy of the heart-brain axis remains to be completely understood. Here, we elucidate the potential effects of myocardial injury on pathways and inflammatory mediators responsible for cognitive impairment using a rodent myocardial injury model. The results demonstrate direct extracellular vesicle (EV)-mediated heart-brain crosstalk and the glial uptake of cardiac EVs. In addition, brain inflammation was also elicited following myocardial injury. Moreover, cardiac EVs promote brain microglial cell activation in vitro, potentially mediated by EV-enriched micro-RNAs (miRNAs). miRNA-21 was selectively up-regulated and secreted by cardiac cells under stress via EVs and contributed to a proinflammatory response in microglia in vitro. Under cardiac stress, cardiac-secreted EVs abundant with miRNA-21 communicate with the brain and are associated with microglial activation, which may be responsible for neuroinflammation and neurotoxicity following myocardial injury.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 7","pages":"Article 101307"},"PeriodicalIF":8.4,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144365070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Smells Like Therapy: Targeting Sulfur Signaling in Cardiometabolic HFpEF. 气味疗法：在心脏代谢HFpEF中靶向硫信号。
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-06-23 DOI: 10.1016/j.jacbts.2025.101316
Rongling Wang, Gabriele G Schiattarella
{"title":"Smells Like Therapy: Targeting Sulfur Signaling in Cardiometabolic HFpEF.","authors":"Rongling Wang, Gabriele G Schiattarella","doi":"10.1016/j.jacbts.2025.101316","DOIUrl":"https://doi.org/10.1016/j.jacbts.2025.101316","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101316"},"PeriodicalIF":8.4,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144794468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Combining Genetic Tools to Determine Lipoprotein(a) Concentrations and Their Associated Cardiovascular Risks Across Different Ethnicities. 结合遗传工具测定不同种族的脂蛋白(a)浓度及其相关心血管风险
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-06-23 DOI: 10.1016/j.jacbts.2025.101315
Raul D Santos
{"title":"Combining Genetic Tools to Determine Lipoprotein(a) Concentrations and Their Associated Cardiovascular Risks Across Different Ethnicities.","authors":"Raul D Santos","doi":"10.1016/j.jacbts.2025.101315","DOIUrl":"https://doi.org/10.1016/j.jacbts.2025.101315","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101315"},"PeriodicalIF":8.4,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
ATP-Citrate Lyase Supports Cardiac Function and NAD+/NADH Balance and Is Depressed in Human Failing Myocardium atp -柠檬酸解酶支持心功能和NAD+/NADH平衡，并在人类衰竭心肌中被抑制
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-06-10 DOI: 10.1016/j.jacbts.2025.04.015
Mariam Meddeb MD , Navid Koleini MD, PhD , Mohammad Keykhaei MD , Ting Liu PhD , Marcus Rhodehamel BA , Lorena Mandarano BS , Farnaz Farshidfar MD , Liang Zhao PhD , Seoyoung Kwon BS , Gizem Keceli PhD , Ismayil Ahmet PhD , Nazareno Paolocci MD, PhD , Virginia Hahn MD , Kavita Sharma MD , Erika L. Pearce PhD , David A. Kass MD
{"title":"ATP-Citrate Lyase Supports Cardiac Function and NAD+/NADH Balance and Is Depressed in Human Failing Myocardium","authors":"Mariam Meddeb MD ,&nbsp;Navid Koleini MD, PhD ,&nbsp;Mohammad Keykhaei MD ,&nbsp;Ting Liu PhD ,&nbsp;Marcus Rhodehamel BA ,&nbsp;Lorena Mandarano BS ,&nbsp;Farnaz Farshidfar MD ,&nbsp;Liang Zhao PhD ,&nbsp;Seoyoung Kwon BS ,&nbsp;Gizem Keceli PhD ,&nbsp;Ismayil Ahmet PhD ,&nbsp;Nazareno Paolocci MD, PhD ,&nbsp;Virginia Hahn MD ,&nbsp;Kavita Sharma MD ,&nbsp;Erika L. Pearce PhD ,&nbsp;David A. Kass MD","doi":"10.1016/j.jacbts.2025.04.015","DOIUrl":"10.1016/j.jacbts.2025.04.015","url":null,"abstract":"<div><div>ATP-citrate lyase (ACLY) regulates lipogenesis and cell proliferation, and forms a cytosolic TCA-bypass circuit impacting NADH. We show that acute and chronic ACLY inhibition in cardiomyocytes depresses the NAD<sup>+</sup>/NADH ratio by increasing mitochondrial NADH. Acute suppression causes dose-dependent cytotoxicity, but at low doses augments aerobic respiration without impeding myocyte function. ACLY is reduced in human failing myocardium, and mice with myocardial or myocyte ACLY knockdown display mildly depressed function, particularly after pressure-overload, and exertional limitations. NAD+ enhancement ameliorates dysfunction/toxicity from ACLY inhibition. These results reveal that ACLY intrinsically regulates cardiac NAD<sup>+</sup>/NADH balance and respiration, which can affect rest and reserve heart function.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 7","pages":"Article 101301"},"PeriodicalIF":8.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144253314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Ufmylation Suppresses Unfolded Protein Response to Prevent Peripartum Cardiomyopathy. ufmyation抑制未折叠蛋白反应预防围产期心肌病。
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-06-04 DOI: 10.1016/j.jacbts.2025.04.007
Varsha Tandra, Lingxian Zhang, Chang Min Lee, Yongbing Wu, Guihua Yue, Honglin Li, Huabo Su, Jie Li
{"title":"Ufmylation Suppresses Unfolded Protein Response to Prevent Peripartum Cardiomyopathy.","authors":"Varsha Tandra, Lingxian Zhang, Chang Min Lee, Yongbing Wu, Guihua Yue, Honglin Li, Huabo Su, Jie Li","doi":"10.1016/j.jacbts.2025.04.007","DOIUrl":"https://doi.org/10.1016/j.jacbts.2025.04.007","url":null,"abstract":"<p><p>Ufmylation is a novel ubiquitin-like protein modification that plays a critical role in maintaining the homeostasis of different tissues, but its role in the heart remains poorly understood. Here, we showed that mice lacking UFM1 ligase 1 (UFL1), an enzyme essential for ufmylation, in the heart developed peripartum cardiomyopathy. Loss of UFL1 reversed pregnancy-induced adaptive cardiac transcriptome alterations. Moreover, loss of UFL1 triggered excessive endoplasmic reticulum stress, inhibited mitochondrial oxidative metabolism, and caused augmented mTOR signaling, leading to pronounced pathological remodeling and heart failure. These results demonstrate that ufmylation is essential for physiological cardiac remodeling and that disruption of ufmylation predisposes the heart to peripartum cardiomyopathy.</p>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101293"},"PeriodicalIF":8.4,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Hydrogen Sulfide Deficiency and Therapeutic Targeting in Cardiometabolic HFpEF: Evidence for Synergistic Benefit With GLP-1/Glucagon Agonism. 硫化氢缺乏和心脏代谢性HFpEF的治疗靶向：GLP-1/胰高血糖素激动剂协同效应的证据。
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-06-04 DOI: 10.1016/j.jacbts.2025.04.011
Jake E Doiron, Mahmoud H Elbatreek, Huijing Xia, Xiaoman Yu, Natalie D Gehred, Tatiana Gromova, Jingshu Chen, Ian H Driver, Naoto Muraoka, Martin Jensen, Smitha Shambhu, W H Wilson Tang, Kyle B LaPenna, Thomas E Sharp, Traci T Goodchild, Ming Xian, Shi Xu, Heather Quiriarte, Timothy D Allerton, Alexia Zagouras, Jennifer Wilcox, Sanjiv J Shah, Josef Pfeilschifter, Karl-Friedrich Beck, Thomas M Vondriska, Zhen Li, David J Lefer
{"title":"Hydrogen Sulfide Deficiency and Therapeutic Targeting in Cardiometabolic HFpEF: Evidence for Synergistic Benefit With GLP-1/Glucagon Agonism.","authors":"Jake E Doiron, Mahmoud H Elbatreek, Huijing Xia, Xiaoman Yu, Natalie D Gehred, Tatiana Gromova, Jingshu Chen, Ian H Driver, Naoto Muraoka, Martin Jensen, Smitha Shambhu, W H Wilson Tang, Kyle B LaPenna, Thomas E Sharp, Traci T Goodchild, Ming Xian, Shi Xu, Heather Quiriarte, Timothy D Allerton, Alexia Zagouras, Jennifer Wilcox, Sanjiv J Shah, Josef Pfeilschifter, Karl-Friedrich Beck, Thomas M Vondriska, Zhen Li, David J Lefer","doi":"10.1016/j.jacbts.2025.04.011","DOIUrl":"10.1016/j.jacbts.2025.04.011","url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) presents significant treatment challenges. We assessed hydrogen sulfide (H<sub>2</sub>S) bioavailability in HFpEF patients and 2 animal models: the \"2-hit\" L-NAME + high-fat diet mouse model and ZSF1 obese rats. H<sub>2</sub>S levels were significantly reduced in patients and both models, linked to decreased cystathionine-γ-lyase expression and increased sulfide quinone oxidoreductase. Cystathionine-γ-lyase knockout worsened HFpEF, whereas pharmacological supplementation with an H<sub>2</sub>S donor improved diastolic function and reduced cardiac fibrosis. H<sub>2</sub>S supplement synergized with GLP-1/glucagon agonist and ameliorated HFpEF. These findings suggest that enhancing H<sub>2</sub>S bioavailability may provide a novel therapeutic strategy for HFpEF.</p>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101297"},"PeriodicalIF":8.4,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144794466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Nonstructural Roles of Junctophilin-2 in the Heart. 结膜亲蛋白-2在心脏中的非结构作用。
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-06-04 DOI: 10.1016/j.jacbts.2025.03.004
Daniel F Hutchison, Satadru K Lahiri, Kurt W Prins, Xander H T Wehrens
{"title":"Nonstructural Roles of Junctophilin-2 in the Heart.","authors":"Daniel F Hutchison, Satadru K Lahiri, Kurt W Prins, Xander H T Wehrens","doi":"10.1016/j.jacbts.2025.03.004","DOIUrl":"10.1016/j.jacbts.2025.03.004","url":null,"abstract":"<p><p>Junctophilin-2 (JPH2) is an essential structural protein that maintains the integrity of junctional membrane complexes (JMCs) in cardiomyocytes, thereby playing its canonical role in excitation-contraction (E-C) coupling. Recent studies reveal novel, nonstructural functions of JPH2 in cardiomyocytes, including regulation of mitochondrial function, lipid metabolism, nuclear signaling, and innate immune responses. Calpain-mediated cleavage of JPH2 generates nuclear fragments, which differentially modulate stress responses. Moreover, full-length JPH2 also localizes to the nucleus, where it forms phase-separated nuclear droplets during oxidative stress. Collectively, these findings highlight JPH2 as a multifunctional protein with critical roles beyond its canonical structural function in E-C coupling.</p>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101272"},"PeriodicalIF":8.4,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Novel Peptide Therapeutics Targeting the L-Type Calcium Channel Prevent Hypertrophic Cardiomyopathy by Decreasing Mitochondrial Energetics. 针对l型钙通道的新型肽疗法通过降低线粒体能量来预防肥厚性心肌病。
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-06-04 DOI: 10.1016/j.jacbts.2025.04.006
Teagan S Er, Daniel Reinke, Alice J Francis, Tanya M Solomon, Helena M Viola, Henrietta Cserne Szappanos, Caitlyn M Richworth, Catherine Jenkins, Juan E Camacho Londoño, Padmapriya Ponnuswamy, Ciaran McFarlane, Filip Van Petegem, Livia C Hool
{"title":"Novel Peptide Therapeutics Targeting the L-Type Calcium Channel Prevent Hypertrophic Cardiomyopathy by Decreasing Mitochondrial Energetics.","authors":"Teagan S Er, Daniel Reinke, Alice J Francis, Tanya M Solomon, Helena M Viola, Henrietta Cserne Szappanos, Caitlyn M Richworth, Catherine Jenkins, Juan E Camacho Londoño, Padmapriya Ponnuswamy, Ciaran McFarlane, Filip Van Petegem, Livia C Hool","doi":"10.1016/j.jacbts.2025.04.006","DOIUrl":"https://doi.org/10.1016/j.jacbts.2025.04.006","url":null,"abstract":"<p><p>Mitochondrial dysfunction is considered to drive the development of hypertrophic cardiomyopathy (HCM). In search of a preventative HCM therapy, we explored the efficacy of amino acid peptide variants that could alter the L-type Ca<sup>2+</sup> channel's regulation of mitochondrial energetics. We confirmed that 3 of the 4 variant peptides bound with high affinity to the beta subunit. In vivo treatment of cTnI-G203S and αMHC<sup>403/+</sup> mice with the peptide variants prevented the development of HCM and improved contractile function. Here, we describe a novel therapy that uniquely targets the L-type Ca<sup>2+</sup> channel to modify mitochondrial function and prevent HCM.</p>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101292"},"PeriodicalIF":8.4,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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