YAP K236 Acetylation Facilitates its Nucleic Export and Deprived the Protection against Cardiac Hypertrophy in Mice DOI Creative Commons

Panxia Wang,

Luping Wang, Cui Liu

и другие.

Pharmacological Research, Год журнала: 2024, Номер 211, С. 107573 - 107573

Опубликована: Дек. 31, 2024

Язык: Английский

Roles of Sirtuins in Cardiovascular Diseases: Mechanisms and Therapeutics DOI

Yang-Nan Ding,

Hui-Yu Wang,

Xiaofeng Chen

и другие.

Circulation Research, Год журнала: 2025, Номер 136(5), С. 524 - 550

Опубликована: Фев. 27, 2025

Cardiovascular diseases (CVDs) are experiencing a rapid surge and widely recognized as the leading cause of mortality in current aging society. Given multifactorial etiology CVDs, understanding intricate molecular cellular mechanisms is imperative. Over past 2 decades, many scientists have focused on Sirtuins, family nicotinamide adenine dinucleotide–dependent deacylases. Sirtuins highly conserved across species, from yeasts to primates, play crucial role linking diseases. participate nearly all key physiological pathological processes, ranging embryogenic development stress response aging. Abnormal expression activity exist aging-related diseases, while their activation has shown efficacy mitigating these (eg, CVDs). In terms research, this field maintained fast, sustained growth recent years, fundamental studies clinical trials. review, we present comprehensive, up-to-date discussion biological functions roles regulating cardiovascular biology CVDs. Furthermore, highlight latest advancements utilizing Sirtuin-activating compounds dinucleotide boosters potential pharmacological targets for preventing treating The unresolved issues field—from chemicobiological regulation Sirtuin-targeted CVD investigations—are also discussed. This timely review could be critical updated knowledge Sirtuin CVDs facilitating accessibility Sirtuin-targeting interventions.

Язык: Английский

Процитировано

3

Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation DOI
Tim Koopmans,

Eva van Rooij

Nature Reviews Cardiology, Год журнала: 2025, Номер unknown

Опубликована: Апрель 7, 2025

Язык: Английский

Процитировано

0

Cardiac enhancers: Gateway to the regulatory mechanisms of heart regeneration DOI

Ian J. Begeman,

Megan E Guyer,

Junsu Kang

и другие.

Seminars in Cell and Developmental Biology, Год журнала: 2025, Номер 170, С. 103610 - 103610

Опубликована: Апрель 10, 2025

Язык: Английский

Процитировано

0

β-adrenergic receptor inhibits heart regeneration by downregulating Yap m6A modification DOI Creative Commons

Kaihang Guan,

Zijian Li

Cell Death and Disease, Год журнала: 2025, Номер 16(1)

Опубликована: Апрель 14, 2025

Abstract Newborn mammals transiently maintain the heart regenerative capacity. β-adrenergic receptor (β-AR) is most critical in regulating cardiomyocyte behavior. However, role and mechanism of β-AR, especially subtypes regeneration remain unclear. Here, we reveal that β-AR inhibits by downregulating Yap m6A modification. The expression associated with After apical resection, (including β 1 -AR 2 -AR) regeneration. exerts a more potent inhibitory effect compared -AR. Mechanistically, both downregulate modification then YAP differentially reducing METTL14 IGF2BP1, respectively. Elevation adenoviruses encoding IGF2BP1 rescues proliferation inhibited -AR, These findings indicate inhibit m6A-dependent manner subtype-specific mechanism. results will provide new intervention strategy for

Язык: Английский

Процитировано

0

The effects of YAP/TAZ in cardiomyocytes: a scoping review DOI
Yenni Limyati, Ardo Sanjaya, Rafael Sebastián

и другие.

Molecular Biology Reports, Год журнала: 2025, Номер 52(1)

Опубликована: Апрель 15, 2025

Язык: Английский

Процитировано

0

Dysfunctional cardiomyocyte signalling and heart disease DOI Creative Commons

Zara Ridgway,

Xuan Li

Current Opinion in Cell Biology, Год журнала: 2025, Номер 94, С. 102517 - 102517

Опубликована: Апрель 17, 2025

Cardiomyocyte signalling pathways are central to maintaining the structural and functional integrity of heart. Dysregulation these contributes onset progression heart diseases, including failure, arrhythmias cardiomyopathies. This review focuses on very recent work dysfunctional cardiomyocyte its role in pathophysiology disease. We discuss key pathways, immune within cardiomyocytes, associated with microtubule dysfunction, Hippo-yes-associated protein adenosine monophosphate-activated kinase signalling, highlighting how aberrations their regulation lead impaired functions pinpointing potential therapeutic opportunities pathways. underscores complexity networks emphasises need for further dissecting prevent dysfunction.

Язык: Английский

Процитировано

0

E-cadherin inhibits the proliferation and migration of human colorectal cancer cells through Hippo signaling pathway DOI Creative Commons
Zhijin Wang,

Xiaohua Qin,

Shanshan Liu

и другие.

European Journal of Histochemistry, Год журнала: 2025, Номер 69(2)

Опубликована: Май 26, 2025

E-cadherin (E-cad) is a crucial regulatory factor in rescue Epithelial-mesenchymal transition and involved the occurrence of various malignant tumor. However, mechanisms by which regulates tumor metastasis CRC remain unclear. We established sh-E-cad (silenced short hairpin RNA) rescue-E-cad (overexpressed E-cad plasmid transfection) cell lines to investigate role vitro. Immunohistochemistry, clonogenic assays, scratch wound healing CCK-8 flow cytometry, Transwell assay, real time-PCR Western blot were employed underlying involve progression CRC. In tissues, expression was significantly reduced, while YAP markedly elevated. Silencing induced significant increase ability cells, reduced upon expression. assays indicate that low enhances migration, finding corroborated experiments. results demonstrate silencing promotes proliferation cells. Importantly, we found influences apoptosis rather than cycle. Analysis Hippo signaling pathway-related factors revealed resulted decreased MST1/2 LATS1/2, as well phosphorylation levels YAP, increased. Additionally, immunofluorescence confirmed nuclear translocation YAP. Our study indicates via pathway, offering potential new strategy for treatment.

Язык: Английский

Процитировано

0

Acetyltransferase in cardiovascular disease and aging DOI Open Access
Mariko Aoyagi Keller, Michinari Nakamura

The Journal of Cardiovascular Aging, Год журнала: 2024, Номер 4(4)

Опубликована: Дек. 31, 2024

Acetyltransferases are enzymes that catalyze the transfer of an acetyl group to a substrate, modification referred as acetylation. Loss-of-function variants in genes encoding acetyltransferases can lead congenital disorders, often characterized by intellectual disability and heart muscle defects. Their activity is influenced dietary nutrients alter coenzyme A levels, key cofactor. Cardiovascular diseases, including ischemic, hypertensive, diabetic diseases - leading causes mortality elderly largely attributed prolonged lifespan growing prevalence metabolic syndrome. thus serve crucial link between lifestyle modifications, cardiometabolic disease, aging through both epigenomic non-epigenomic mechanisms. In this review, we discuss roles relevance acetyltransferases. While sirtuin family deacetylases has been extensively studied longevity, particularly fasting-mediated NAD+ metabolism, recent research brought attention essential health aging-related pathways, cell proliferation, DNA damage response, mitochondrial function, inflammation, senescence. We begin with overview acetyltransferases, classifying them domain structure, canonical non-canonical lysine N-terminal sialic acid O-acetyltransferases. then advances understanding acetyltransferase-related pathologies, focusing on cardiovascular disease aging, explore their potential therapeutic applications for promoting older individuals.

Язык: Английский

Процитировано

2

Spotlight on YAP: Unlocking New Insights to Overcome the Barriers to Heart Regeneration DOI
Nivedhitha Velayutham, Richard Lee

Circulation, Год журнала: 2024, Номер 151(1), С. 94 - 97

Опубликована: Дек. 26, 2024

Язык: Английский

Процитировано

0

YAP K236 Acetylation Facilitates its Nucleic Export and Deprived the Protection against Cardiac Hypertrophy in Mice DOI Creative Commons

Panxia Wang,

Luping Wang, Cui Liu

и другие.

Pharmacological Research, Год журнала: 2024, Номер 211, С. 107573 - 107573

Опубликована: Дек. 31, 2024

Язык: Английский

Процитировано

0