@article{MTMT:34815712,
	title = {The cardiovascular changes underlying a low cardiac output with exercise in patients with type 2 diabetes mellitus},
	url = {https://m2.mtmt.hu/api/publication/34815712},
	author = {Madsen, Per Lav and Sejersen, Casper and Nyberg, Michael and Sorensen, Martin Heyn and Hellsten, Ylva and Gaede, Peter and Bojer, Annemie Stege},
	doi = {10.3389/fphys.2024.1294369},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {15},
	unique-id = {34815712},
	abstract = {The significant morbidity and premature mortality of type 2 diabetes mellitus (T2DM) is largely associated with its cardiovascular consequences. Focus has long been on the arterial atheromatosis of DM giving rise to early stroke and myocardial infarctions, whereas less attention has been given to its non-ischemic cardiovascular consequences. Irrespective of ischemic changes, T2DM is associated with heart failure (HF) most commonly with preserved ejection fraction (HFpEF). Largely due to increasing population ages, hypertension, obesity and T2DM, HFpEF is becoming the most prevalent form of heart failure. Unfortunately, randomized controlled trials of HFpEF have largely been futile, and it now seems logical to address the important different phenotypes of HFpEF to understand their underlying pathophysiology. In the early phases, HFpEF is associated with a significantly impaired ability to increase cardiac output with exercise. The lowered cardiac output with exercise results from both cardiac and peripheral causes. T2DM is associated with left ventricular (LV) diastolic dysfunction based on LV hypertrophy with myocardial disperse fibrosis and significantly impaired ability for myocardial blood flow increments with exercise. T2DM is also associated with impaired ability for skeletal muscle vasodilation during exercise, and as is the case in the myocardium, such changes may be related to vascular rarefaction. The present review discusses the underlying phenotypical changes of the heart and peripheral vascular system and their importance for an adequate increase in cardiac output. Since many of the described cardiovascular changes with T2DM must be considered difficult to change if fully developed, it is suggested that patients with T2DM are early evaluated with respect to their cardiovascular compromise.},
	keywords = {NITRIC-OXIDE; CONGESTIVE-HEART-FAILURE; HYPERTENSION; type 2 diabetes mellitus; HUMAN SKELETAL-MUSCLE; LEFT-VENTRICULAR HYPERTROPHY; PULSE-WAVE VELOCITY; Exercise intolerance; Cardiac fibrosis; ISOLATED SYSTOLIC HYPERTENSION; heart failure with a preserved ejection fraction; REDUCES ARTERIAL STIFFNESS; LIFELONG PHYSICAL-ACTIVITY; BLOOD-FLOW REGULATION},
	year = {2024},
	eissn = {1664-042X}
}

@article{MTMT:34815350,
	title = {Uridine and its role in metabolic diseases, tumors, and neurodegenerative diseases},
	url = {https://m2.mtmt.hu/api/publication/34815350},
	author = {Yang, Y. and Ye, Y. and Deng, Y. and Gao, L.},
	doi = {10.3389/fphys.2024.1360891},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {15},
	unique-id = {34815350},
	year = {2024},
	eissn = {1664-042X}
}

@article{MTMT:34801055,
	title = {Pleiotropic physiological functions of Piezo1 in human body and its effect on malignant behavior of tumors},
	url = {https://m2.mtmt.hu/api/publication/34801055},
	author = {Zhang, Yihan and Zou, Wen and Dou, Wenlei and Luo, Hongliang and Ouyang, Xi},
	doi = {10.3389/fphys.2024.1377329},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {15},
	unique-id = {34801055},
	abstract = {Mechanosensitive ion channel protein 1 (Piezo1) is a large homotrimeric membrane protein. Piezo1 has various effects and plays an important and irreplaceable role in the maintenance of human life activities and homeostasis of the internal environment. In addition, recent studies have shown that Piezo1 plays a vital role in tumorigenesis, progression, malignancy and clinical prognosis. Piezo1 is involved in regulating the malignant behaviors of a variety of tumors, including cellular metabolic reprogramming, unlimited proliferation, inhibition of apoptosis, maintenance of stemness, angiogenesis, invasion and metastasis. Moreover, Piezo1 regulates tumor progression by affecting the recruitment, activation, and differentiation of multiple immune cells. Therefore, Piezo1 has excellent potential as an anti-tumor target. The article reviews the diverse physiological functions of Piezo1 in the human body and its major cellular pathways during disease development, and describes in detail the specific mechanisms by which Piezo1 affects the malignant behavior of tumors and its recent progress as a new target for tumor therapy, providing new perspectives for exploring more potential effects on physiological functions and its application in tumor therapy.},
	keywords = {TUMOR; METASTASIS; THERAPEUTIC TARGET; PIEZO1; initiation and progression},
	year = {2024},
	eissn = {1664-042X}
}

@article{MTMT:34797930,
	title = {Motor properties of Myosin 5c are modulated by tropomyosin isoforms and inhibited by pentabromopseudilin},
	url = {https://m2.mtmt.hu/api/publication/34797930},
	author = {Kengyel, András Miklós and Palarz, Philip M and Krohn, Jacqueline and Marquardt, Anja and Greve, Johannes N and Heiringhoff, Robin and Jörns, Anne and Manstein, Dietmar J},
	doi = {10.3389/fphys.2024.1394040},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {15},
	unique-id = {34797930},
	abstract = {Myosin 5c (Myo5c) is a motor protein that is produced in epithelial and glandular tissues, where it plays an important role in secretory processes. Myo5c is composed of two heavy chains, each containing a generic motor domain, an elongated neck domain consisting of a single α-helix with six IQ motifs, each of which binds to a calmodulin (CaM) or a myosin light chain from the EF-hand protein family, a coiled-coil dimer-forming region and a carboxyl-terminal globular tail domain. Although Myo5c is a low duty cycle motor, when two or more Myo5c-heavy meromyosin (HMM) molecules are linked together, they move processively along actin filaments. We describe the purification and functional characterization of human Myo5c-HMM co-produced either with CaM alone or with CaM and the essential and regulatory light chains Myl6 and Myl12b. We describe the extent to which cofilaments of actin and Tpm1.6, Tpm1.8 or Tpm3.1 alter the maximum actin-activated ATPase and motile activity of the recombinant Myo5c constructs. The small allosteric effector pentabromopseudilin (PBP), which is predicted to bind in a groove close to the actin and nucleotide binding site with a calculated ΔG of -18.44 kcal/mol, inhibits the motor function of Myo5c with a half-maximal concentration of 280 nM. Using immunohistochemical staining, we determined the distribution and exact localization of Myo5c in endothelial and endocrine cells from rat and human tissue. Particular high levels of Myo5c were observed in insulin-producing β-cells located within the pancreatic islets of Langerhans.},
	keywords = {immunohistochemistry; Molecular docking; tropomyosin; pentabromopseudilin; Myosin 5c},
	year = {2024},
	eissn = {1664-042X}
}

@article{MTMT:34797875,
	title = {miR-146a is a critical target associated with multiple biological pathways of skin aging},
	url = {https://m2.mtmt.hu/api/publication/34797875},
	author = {Stafa, Klodjan and Rella, Antonella and Eagle, Whitby and Dong, Kelly and Morris, Kelsey and Layman, Dawn and Corallo, Krystle and Trivero, Jacqueline and Maidhof, Robert and Goyarts, Earl and Pernodet, Nadine},
	doi = {10.3389/fphys.2024.1291344},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {15},
	unique-id = {34797875},
	year = {2024},
	eissn = {1664-042X}
}

@article{MTMT:34794594,
	title = {Effect of active and passive techniques used in thromboembolic prophylaxis on venous flow velocity in the post-procedure period},
	url = {https://m2.mtmt.hu/api/publication/34794594},
	author = {Zsenák, István and Makai, Alexandra and Kiss, Gabriella and Faludi, Béla and Straub, Alexandra and Szilágyi, Brigitta and Velényi, Anita and Járomi, Melinda},
	doi = {10.3389/fphys.2024.1323840},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {15},
	unique-id = {34794594},
	year = {2024},
	eissn = {1664-042X},
	orcid-numbers = {Makai, Alexandra/0000-0002-1907-120X}
}

@article{MTMT:34789065,
	title = {Polyphenol supplementation boosts aerobic endurance in athletes: systematic review},
	url = {https://m2.mtmt.hu/api/publication/34789065},
	author = {Cao, Gexin and Zuo, Jing and Wu, Baile and Wu, Ying},
	doi = {10.3389/fphys.2024.1369174},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {15},
	unique-id = {34789065},
	abstract = {In recent years, an increasing trend has been observed in the consumption of specific polyphenols, such as flavonoids and phenolic acids, derived from green tea, berries, and other similar sources. These compounds are believed to alleviate oxidative stress and inflammation resulting from exercise, potentially enhancing athletic performance. This systematic review critically examines the role of polyphenol supplementation in improving aerobic endurance among athletes and individuals with regular exercise habits. The review involved a thorough search of major literature databases, including PubMed, Web of Science, SCOPUS, SPORTDiscus, and Embase, covering re-search up to the year 2023. Out of 491 initially identified articles, 11 met the strict inclusion criteria for this review. These studies specifically focused on the incorporation of polyphenols or polyphenol-containing complexes in their experimental design, assessing their impact on aerobic endurance. The methodology adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and the risk of bias was evaluated using the Cochrane bias risk assessment tool. While this review suggests that polyphenol supplementation might enhance certain aspects of aerobic endurance and promote fat oxidation, it is important to interpret these findings with caution, considering the limited number of studies available.},
	year = {2024},
	eissn = {1664-042X},
	pages = {1-18}
}

@article{MTMT:34785754,
	title = {Fibrosis modeling choice affects morphology of ventricular arrhythmia in non-ischemic cardiomyopathy},
	url = {https://m2.mtmt.hu/api/publication/34785754},
	author = {Myklebust, Lena and Maleckar, Mary M. and Arevalo, Hermenegild},
	doi = {10.3389/fphys.2024.1370795},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {15},
	unique-id = {34785754},
	abstract = {Introduction: Patients with non-ischemic cardiomyopathy (NICM) are at risk for ventricular arrhythmias, but diagnosis and treatment planning remain a serious clinical challenge. Although computational modeling has provided valuable insight into arrhythmic mechanisms, the optimal method for simulating reentry in NICM patients with structural disease is unknown. Methods: Here, we compare the effects of fibrotic representation on both reentry initiation and reentry morphology in patient-specific cardiac models. We investigate models with heterogeneous networks of non-conducting structures (cleft models) and models where fibrosis is represented as a dense core with a surrounding border zone (non-cleft models). Using segmented cardiac magnetic resonance with late gadolinium enhancement (LGE) of five NICM patients, we created 185 3D ventricular electrophysiological models with different fibrotic representations (clefts, reduced conductivity and ionic remodeling). Results: Reentry was induced by electrical pacing in 647 out of 3,145 simulations. Both cleft and non-cleft models can give rise to double-loop reentries meandering through fibrotic regions (Type 1-reentry). When accounting for fibrotic volume, the initiation sites of these reentries are associated with high local fibrotic density (mean LGE in cleft models: p < 0.001, core volume in non-cleft models: p = 0.018, negative binomial regression). In non-cleft models, Type 1-reentries required slow conduction in core tissue (non-clefts c models) as opposed to total conduction block. Incorporating ionic remodeling in fibrotic regions can give rise to single- or double-loop rotors close to healthy-fibrotic interfaces (Type 2-reentry). Increasing the cleft density or core-to-border zone ratio in cleft and non-cleft c models, respectively, leads to increased inducibility and a change in reentry morphology from Type 2 to Type 1. Conclusions: By demonstrating how fibrotic representation affects reentry morphology and location, our findings can aid model selection for simulating arrhythmogenesis in NICM.},
	keywords = {SUBSTRATE; IDENTIFICATION; MORTALITY; tachycardia; HEART-DISEASE; DILATED CARDIOMYOPATHY; myocardial fibrosis; Cardiac fibrosis; computational electrophysiology; Interstitial fibrosis; Patient-Specific Modeling; electrical heterogeneity; non-ischemic cardiomyopathy; re-entrant arrhythmia; SCAR CHARACTERIZATION; late gadolinium enhanced magnetic resonance imaging},
	year = {2024},
	eissn = {1664-042X}
}

@article{MTMT:34781515,
	title = {Understanding bovine embryo elongation: a transcriptomic study of trophoblastic vesicles},
	url = {https://m2.mtmt.hu/api/publication/34781515},
	author = {Degrelle, S.A. and Liu, F. and Laloe, D. and Richard, C. and Le, Bourhis D. and Rossignol, M.-N. and Hue, I.},
	doi = {10.3389/fphys.2024.1331098},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {15},
	unique-id = {34781515},
	year = {2024},
	eissn = {1664-042X}
}

@article{MTMT:34781057,
	title = {Identification of a shared gene signature and biological mechanism between diabetic foot ulcers and cutaneous lupus erythemnatosus by transcriptomic analysis},
	url = {https://m2.mtmt.hu/api/publication/34781057},
	author = {Wu, S. and Wang, Y. and Duan, J. and Teng, Y. and Wang, D. and Qi, F.},
	doi = {10.3389/fphys.2024.1297810},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {15},
	unique-id = {34781057},
	abstract = {Diabetic foot ulcers (DFU) and cutaneous lupus erythematosus (CLE) are both diseases that can seriously affect a patient’s quality of life and generate economic pressure in society. Symptomatically, both DLU and CLE exhibit delayed healing and excessive inflammation; however, there is little evidence to support a molecular and cellular connection between these two diseases. In this study, we investigated potential common characteristics between DFU and CLE at the molecular level to provide new insights into skin diseases and regeneration, and identify potential targets for the development of new therapies. The gene expression profiles of DFU and CLE were obtained from the Gene Expression Omnibus (GEO) database and used for analysis. A total of 41 common differentially expressed genes (DEGs), 16 upregulated genes and 25 downregulated genes, were identified between DFU and CLE. GO and KEGG analysis showed that abnormalities in epidermal cells and the activation of inflammatory factors were both involved in the occurrence and development of DFU and CLE. Protein-protein interaction network (PPI) and sub-module analysis identified enrichment in seven common key genes which is KRT16, S100A7, KRT77, OASL, S100A9, EPGN and SAMD9. Based on these seven key genes, we further identified five miRNAs(has-mir-532-5p, has-mir-324-3p,has-mir-106a-5p,has-mir-20a-5p,has-mir-93-5p) and7 transcription factors including CEBPA, CEBPB, GLI1, EP30D, JUN,SP1, NFE2L2 as potential upstream molecules. Functional immune infiltration assays showed that these genes were related to immune cells. The CIBERSORT algorithm and Pearson method were used to determine the correlations between key genes and immune cells, and reverse key gene-immune cell correlations were found between DFU and CLE. Finally, the DGIbd database demonstrated that Paquinimod and Tasquinimod could be used to target S100A9 and Ribavirin could be used to target OASL. Our findings highlight common gene expression characteristics and signaling pathways between DFU and CLE, indicating a close association between these two diseases. This provides guidance for the development of targeted therapies and mutual interactions. Copyright © 2024 Wu, Wang, Duan, Teng, Wang and Qi.},
	keywords = {ARTICLE; PREDICTION; human; Quality of Life; genetic analysis; Gene Expression; Gene Expression Profiling; GENE ONTOLOGY; protein expression; cell activation; immune response; protein protein interaction; gene identification; transcriptomics; protein c jun; down regulation; skin lupus erythematosus; bioinformatics; bioinformatics; Differential gene expression; transcription factor Sp1; transcription factor Gli1; CLE; KEGG; Diabetic foot ulcer; Diabetic foot ulcer; Gene set enrichment analysis; inflammatory; psoriasin; gene network analysis; Cutaneous lupus erythematosus; calgranulin B; Nrf2 signaling; DFU; common key genes},
	year = {2024},
	eissn = {1664-042X}
}