Article
Cardiac & Cardiovascular Systems
Manon Meerman, Rob Driessen, Nicole C. A. van Engeland, Irith Bergsma, Jacco L. G. Steenhuijsen, David Kozono, Elena Aikawa, Jesper Hjortnaes, Carlijn V. C. Bouten
Summary: The study demonstrates that radiation exposure enhances the calcific response in VICs, contributing to the development of valvular disease. High radiation exposure induces the differentiation of VICs into terminally differentiated giant-cell fibroblasts. Further research is needed to uncover the underlying mechanisms of radiation-induced valvular changes.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2021)
Article
Biochemistry & Molecular Biology
Fan Yang, Suxuan Liu, Ying Gu, Yan Yan, Xueyan Ding, Liangjian Zou, Zhiyun Xu, Guokun Wang
Summary: This study reveals that miR-22 plays an important role in promoting the osteogenic differentiation of VICs and accelerating the calcification process in CAVD. The acceleration is achieved through regulating CAB39, the AMPK-mTOR signaling pathway, ROS generation, and autophagic activity.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2022)
Article
Cardiac & Cardiovascular Systems
Chenyang Gao, Wangxing Hu, Feng Liu, Zhiru Zeng, Qifeng Zhu, Jiaqi Fan, Jinyong Chen, Si Cheng, Kaixiang Yu, Yi Qian, Tanchen Ren, Jing Zhao, Xianbao Liu, Jian'an Wang
Summary: This study demonstrates that inhibition of Akr1B1 can attenuate calcification degree both in vitro and in vivo. The Akr1B1 inhibitor epalrestat may be a potential treatment option for CAVD.
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Geanina Voicu, Daniela Rebleanu, Cristina Ana Mocanu, Gabriela Tanko, Ionel Droc, Cristina Mariana Uritu, Mariana Pinteala, Ileana Manduteanu, Maya Simionescu, Manuela Calin
Summary: This study designed and obtained targeted lipid-enveloped polyplexes (V-LPP/shRunx2) suitable for systemic administration and targeted delivery of shRunx2 to osteoblast-differentiated VIC cells. The lipopolyplexes were shown to be cyto- and hemo-compatible, and specifically taken up by osteoblast-differentiated VIC cells. They successfully downregulated the expression of osteogenic molecules and could be a potential nanomedicine approach for blocking the progression of CAVD.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Medicine, Research & Experimental
Li Shu, Zhen Yuan, Fei Li, Zhejun Cai
Summary: Calcified aortic valve disease (CAVD) is a progressive cardiovascular disease involving multiple mechanisms, rather than simply a degenerative disease. Aortic valve endothelial cells (VECs), which are directly exposed to pathogenic factors, play a significant role in the onset and progression of CAVD. Hemodynamic changes damage VECs, leading to inflammatory infiltration and oxidative stress, promoting CAVD progression. VECs also regulate the pathological differentiation of valvular interstitial cells (VICs) and eventually lead to calcification.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Biochemistry & Molecular Biology
Mihaela Vadana, Sergiu Cecoltan, Letitia Ciortan, Razvan D. Macarie, Andreea C. Mihaila, Monica M. Tucureanu, Ana-Maria Gan, Maya Simionescu, Ileana Manduteanu, Ionel Droc, Elena Butoi
Summary: This study found that parathyroid hormone (PTH) can cause dysfunction of human valvular endothelial cells (VEC), which in turn affects the transformation of valvular interstitial cells (VIC) into osteoblast-like cells. These findings shed light on the mechanisms of PTH involvement in valvular calcification pathology and suggest that PTH and treatment of hyperparathyroidism can be a therapeutic strategy to reduce valvular calcification.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Cardiac & Cardiovascular Systems
Chang Hu, Qian Wang, Hui Xue, Hao Hong, Jiawei Shi, Nianguo Dong, Mingkui Zhang
Summary: This study aimed to explore the pathomechanism of human myxomatous valve degeneration by investigating changes in valvular cells, extracellular matrix metabolism, and mechanical properties. The results showed that myxomatous valves have looser and less coordinated extracellular matrices, activated interstitial cells, and disrupted balance between MMP/TIMP.
REVIEWS IN CARDIOVASCULAR MEDICINE
(2021)
Review
Biochemistry & Molecular Biology
Anna Di Vito, Annalidia Donato, Ivan Presta, Teresa Mancuso, Francesco Saverio Brunetti, Pasquale Mastroroberto, Andrea Amorosi, Natalia Malara, Giuseppe Donato
Summary: Calcific Aortic Valve Disease (CAVD) is the most common valvular heart disease in the ageing population, which is strongly correlated with active and degenerative processes. The progression of the disease is closely related to the cellular and matrix alterations within the aortic valve.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Engineering, Biomedical
Amadeus S. Zhu, Tasneem Mustafa, Jennifer P. Connell, K. Jane Grande-Allen
Summary: Mitral valve disease is a common cardiovascular condition characterized by fibrotic remodeling. In this study, it was found that pro-inflammatory cytokines TNF-alpha and IL-1 beta can downregulate myofibroblast differentiation in mitral VICs via the NF-kappa B signaling pathway, suggesting potential new avenues for pharmaceutical treatments for mitral valve disease.
ACTA BIOMATERIALIA
(2021)
Article
Multidisciplinary Sciences
Faye Wang, Cindy Zhang, Jae Kwagh, Brian Strassle, Jinqing Li, Minxue Huang, Yunling Song, Brenda Lehman, Richard Westhouse, Kamalavenkatesh Palanisamy, Vinay K. Holenarsipur, Robert Borzilleri, Karen Augustine-Rauch
Summary: This study showed that the selectivity of TGF beta receptors may influence the potency of valvular toxicity, with dual TGF beta RI/-RII inhibitors having the most profound effect on VIC phenotype.
Article
Immunology
Li Zeng, Yiping Tang, Yichen Zhang, Li Yue, Gang Ma, Xumin Ye, Lijing Yang, Kai Chen, Qiao Zhou
Summary: Through bioinformatics analysis, we identified common hub genes and shared molecular pathways underlying DM and IPF, providing valuable insights into the intricate mechanisms of these diseases and offering potential targets for diagnosis and therapeutic interventions.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Multidisciplinary Sciences
Nozomi Igarashi, Megumi Honjo, Makoto Aihara
Summary: mTOR inhibitors effectively reduce the fibrotic response induced by TGF-beta 2 in cultured human trabecular meshwork cells, as well as decreasing the migration rate of the cells. Further studies are needed to explore the effectiveness of these inhibitors in in vivo models.
SCIENTIFIC REPORTS
(2021)
Article
Cardiac & Cardiovascular Systems
Victoria Nelson, Vaidehi Patil, LaTonya R. Simon, Kelsey Schmidt, Chloe M. McCoy, Kristyn S. Masters
Summary: Valvular interstitial cells regulate the behavior of angiogenic valvular endothelial cells through the secretion of paracrine molecules, which are influenced by cell phenotype and sex. The study reveals differences in the production of pro-angiogenic factors by male and female VICs, as well as varying impacts on endothelial cells based on sex.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2021)
Article
Multidisciplinary Sciences
Cassandra L. Clift, Yan Ru Su, David Bichell, Heather C. Jensen Smith, Jennifer R. Bethard, Kim Norris-Caneda, Susana Comte-Walters, Lauren E. Ball, M. A. Hollingsworth, Anand S. Mehta, Richard R. Drake, Peggi M. Angel
Summary: This study investigates collagen fiber production and regulation in human AV development and pediatric end-stage CAVS by combining histological studies with high resolution accurate mass (HRAM) collagen-targeting proteomics. Specific collagen peptides modified by hydroxylated prolines (HYP) were found to be significantly regulated across patient categories. The study also identified non-collagen type ECM proteins which have direct interactions in collagen synthesis, regulation, or modification, suggesting potential therapeutic avenues for inhibiting valvular degradation and engineered options for valve replacement in pCAVS.
SCIENTIFIC REPORTS
(2021)
Article
Hematology
Nicolas Gendron, Mickael Rosa, Adeline Blandinieres, Yoann Sottejeau, Elisa Rossi, Eric Van Belle, Salim Idelcadi, Severine Lecourt, Andre Vincentelli, Audrey Cras, Ramadan Jashari, Richard Chocron, Yael Baudouin, Thibault Pamart, Ivan Bieche, Nathalie Nevo, Bernard Cholley, Jeanne Rancic, Bart Staels, Pascale Gaussem, Annabelle Dupont, Alain Carpentier, Sophie Susen, David M. Smadja
Summary: The study demonstrated that human VICs isolated from patients with calcific aortic valve disease have the potential to participate in aortic valve angiogenesis by differentiating into perivascular cells and exerting paracrine effects of VEGF-A. These findings suggest a novel function of VICs in valve vascularization during calcific aortic valve disease and highlight the importance of targeting perivascular differentiation and VEGF-A in slowing disease progression.
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
(2021)