Ana Vukolic

718 total citations
15 papers, 423 citations indexed

About

Ana Vukolic is a scholar working on Molecular Biology, Cardiology and Cardiovascular Medicine and Physiology. According to data from OpenAlex, Ana Vukolic has authored 15 papers receiving a total of 423 indexed citations (citations by other indexed papers that have themselves been cited), including 6 papers in Molecular Biology, 5 papers in Cardiology and Cardiovascular Medicine and 3 papers in Physiology. Recurrent topics in Ana Vukolic's work include Cardiovascular Function and Risk Factors (3 papers), Circadian rhythm and melatonin (2 papers) and Renal and related cancers (2 papers). Ana Vukolic is often cited by papers focused on Cardiovascular Function and Risk Factors (3 papers), Circadian rhythm and melatonin (2 papers) and Renal and related cancers (2 papers). Ana Vukolic collaborates with scholars based in Switzerland, France and United Kingdom. Ana Vukolic's co-authors include Jean‐Pierre Montani, Urs Albrecht, Zhihong Yang, Kay‐Dietrich Wagner, Jean‐François Michiels, Vladan Antic, Bruce N. Van Vliet, Nicole Wagner, Delphine Baudouy and Cédric Cortijo and has published in prestigious journals such as Nature, International Journal of Molecular Sciences and European Heart Journal.

In The Last Decade

Ana Vukolic

14 papers receiving 417 citations

Peers

Countries citing papers authored by Ana Vukolic

Since Specialization

Citations

This map shows the geographic impact of Ana Vukolic's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Ana Vukolic with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Ana Vukolic more than expected).

Fields of papers citing papers by Ana Vukolic

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Ana Vukolic. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Ana Vukolic. The network helps show where Ana Vukolic may publish in the future.

Co-authorship network of co-authors of Ana Vukolic

This figure shows the co-authorship network connecting the top 25 collaborators of Ana Vukolic. A scholar is included among the top collaborators of Ana Vukolic based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Ana Vukolic. Ana Vukolic is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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15 of 15 papers shown

#	Title	Journal	Authors	Indexed citations
1	Enhanced neoangiogenesis and balance of the immune response mediated by the Wilms' tumor suppressor WT1 favor repair after myocardial infarction	Theranostics	Nicole Wagner, Ana Vukolic et al.	0
2	Antibody-mediated PCSK9 neutralization worsens outcome after bare-metal stent implantation in mice	Vascular Pharmacology	Yustina M. Puspitasari, Stefano Ministrini et al.	1
3	Long-term dietary n3 fatty acid prevents aging-related cardiac diastolic and vascular dysfunction	Vascular Pharmacology	Seyed Soheil Saeedi Saravi, Nicole R. Bonetti et al.	5
4	Long-term dietary supplementation with plant-derived omega-3 fatty acid improves outcome in experimental ischemic stroke	Atherosclerosis	Nicole R. Bonetti, Luca Liberale et al.	11
5	TNF‐α antagonism rescues the effect of ageing on stroke: Perspectives for targeting inflamm‐ageing	European Journal of Clinical Investigation	Luca Liberale, Nicole R. Bonetti et al.	40
6	Implications of the Wilms’ Tumor Suppressor Wt1 in Cardiomyocyte Differentiation	International Journal of Molecular Sciences	Nicole Wagner, Marina Ninkov et al.	15
7	JCAD enhances arterial thrombosis by regulating endothelial plasminogen activator inhibitor-1 and tissue factor expression	European Heart Journal	Luca Liberale, Alexander Akhmedov et al.	1
8	Echocardiographic and Histological Examination of Cardiac Morphology in the Mouse	Journal of Visualized Experiments	Delphine Baudouy, Jean‐François Michiels et al.	23
9	Andersen’s syndrome mutants produce a knockdown of inwardly rectifying K+ channel in mouse skeletal muscle in vivo	Cell and Tissue Research	Dina Simkin, Gaëlle Robin et al.	7
10	Echocardiographic and Histological Examination of Cardiac Morphology in the Mouse	Journal of Visualized Experiments	Delphine Baudouy, Jean‐François Michiels et al.	3
11	Inducible Conditional Vascular-Specific Overexpression of Peroxisome Proliferator-Activated Receptor Beta/Delta Leads to Rapid Cardiac Hypertrophy	PPAR Research	Kay‐Dietrich Wagner, Ana Vukolic et al.	21
12	HIF-driven SF3B1 induces KHK-C to enforce fructolysis and heart disease	Nature	Peter Mirtschink, Jaya Krishnan et al.	131
13	PER2 promotes glucose storage to liver glycogen during feeding and acute fasting by inducing Gys2 PTG and GL expression	Molecular Metabolism	Fabio Zani, Barbara Becattini et al.	66
14	Period2 gene mutant mice show compromised insulin-mediated endothelial nitric oxide release and altered glucose homeostasis	Frontiers in Physiology	João Miguel Carvas, Ana Vukolic et al.	33
15	Role of mutation of the circadian clock gene Per2 in cardiovascular circadian rhythms	American Journal of Physiology-Regulatory, Integrative and Comparative Physiology	Ana Vukolic, Vladan Antic et al.	66

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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