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A review of RUNX2 genetic interactions and their role in cardiovascular disease

Heart Science Journal · Vol. 7 No. 2 (2026) · hlm. 29–35

DOI
10.21776/ub.hsj.2026.007.02.5
ISSN
2721-9984, 2721-9976
Terbit
2026-04-26
Penerbit
Universitas Brawijaya
Bahasa
en
Lisensi
creativecommons.org/licenses/by/4.0

Abstrak

Cardiovascular diseases (CVD) remain the leading cause of global mortality, with underlying factors such as genetics, environment, and lifestyle interacting in complex and multiple ways. Runt-related transcription factor 2 (RUNX2), traditionally associated with osteogenesis, has gained recognition for its critical role in cardiovascular health. RUNX2 contributes to vascular calcification (VC), endothelial dysfunction, and myocardial fibrosis, thereby accelerating CVD progression. Its expression is influenced by multiple upstream regulators relevant to vascular pathology, such as BMP2/SMAD, Wnt/β-catenin, and ERK signaling, along with epigenetic mechanisms and gene-environment interactions such as oxidative stress, hyperglycemia, and dyslipidemia. Genetic variants in RUNX2 and environmental variables including diet and physical inactivity, amplify its activation, worsening VC and cardiovascular risk. RUNX2 reduces endothelial nitric oxide bioavailability, enhances vascular inflammation, and activates profibrotic signaling in cardiac tissue, promoting vascular dysfunction and myocardial remodeling. Circulating RUNX2 levels and genetic variations exhibit potential as diagnostic and predictive indicators for cardiovascular disease. Severalpharmaceutical agents including metformin, empagliflozin, and statins, as well as natural substances such green tea polyphenols and green coffee extract, have demonstrated partial modulatory effects on RUNX2 activity. Moreover, genome-editing tools such as CRISPR-Cas9 present future opportunities for selective RUNX2 targeting. Comprehensive understanding of RUNX2 regulation and its interaction with genetic and environmental factors offers novel opportunities for personalized CVD prevention and treatment approaches through lifestyle modification, pharmacotherapy, and gene-based interventions in the future.

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Rekan penulisOrganisasiArtikel bersama
Anna Fuji RahimahUniversity of Brawijaya18
Cholid Tri TjahjonoUniversity of Brawijaya18
Ardian RizalUniversity of Brawijaya18
Budi SatrijoUniversity of Brawijaya17
Indra PrasetyaUniversity of Brawijaya17
Setyasih AnjarwaniUniversity of Brawijaya16
Novi KurnianingsihUniversity of Brawijaya13
Yoga WaranugrahaUniversity of Brawijaya9
Djanggan SargowoUniversity of Brawijaya9
Sasmojo WiditoUniversity of Brawijaya9
Heny MartiniUniversity of Brawijaya9
Adhika Prastya WikanandaUniversity of Brawijaya4
Tri AstiawatiUniversity of Brawijaya4
Putri Annisa KamilaUniversity of Brawijaya3
Dadang HendrawanUniversity of Brawijaya3
Muhammad Rizki FadlanUniversity of Brawijaya3
Fandy HazzyUniversity of Brawijaya3
Wella KarolinaUniversity of Brawijaya3
Hayla Iqda MillisaniUniversity of Brawijaya3
Oktivani Adelathifa RahmaUniversity of Brawijaya3
Valerinna YogibuanaAfiliasi tidak diketahui3
Veny KurniawatiUniversity of Brawijaya2
Tonny AdriyantoUniversity of Brawijaya2
Jonny Karunia FajarUniversity of Brawijaya2
Olivia HandayaniUniversity of Brawijaya2
Fahmy RusnantaUniversity of Brawijaya2
Fitranti Suciati LaitupaUniversity of Brawijaya2
Oktafin Srywati PamunaUniversity of Brawijaya2
Anna Fuji RahimahAfiliasi tidak diketahui2
Imelda KrisnasariUniversity of Brawijaya2
Ratna PancasariUniversity of Brawijaya2
Ayu Asri Devi AdityawatiUniversity of Brawijaya2
Krishna Ari NugrahaUniversity of Brawijaya2
Seprian WidasmaraUniversity of Brawijaya2
Pawik SupriadiUniversity of Brawijaya2
Wira KimahesaUniversity of Brawijaya2
Cik KahadiUniversity of Brawijaya2

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Sumber metadata: OAI-PMH (metadata jurnal) https://heartscience.ub.ac.id/index.php/heartscience/oai, pertama di-harvest 8 Nov 2026, terakhir terlihat 8 Nov 2026.
Metadata asli (oai_dc) 
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	<dc:title xml:lang="en">A review of RUNX2 genetic interactions and their role in cardiovascular disease</dc:title>
	<dc:creator xml:lang="en">Christine, Anastasia</dc:creator>
	<dc:creator xml:lang="en">Rohman, Mohammad Saifur</dc:creator>
	<dc:creator xml:lang="en">Yogibuana, Valerinna</dc:creator>
	<dc:subject xml:lang="en">RUNX2</dc:subject>
	<dc:subject xml:lang="en">cardiovascular diseases</dc:subject>
	<dc:subject xml:lang="en">vascular calcification</dc:subject>
	<dc:subject xml:lang="en">therapeutic targets</dc:subject>
	<dc:description xml:lang="en">Cardiovascular diseases (CVD) remain the leading cause of global mortality, with underlying factors such as genetics, environment, and lifestyle interacting in complex and multiple ways. Runt-related transcription factor 2 (RUNX2), traditionally associated with osteogenesis, has gained recognition for its critical role in cardiovascular health. RUNX2 contributes to vascular calcification (VC), endothelial dysfunction, and myocardial fibrosis, thereby accelerating CVD progression. Its expression is influenced by multiple upstream regulators relevant to vascular pathology, such as BMP2/SMAD, Wnt/β-catenin, and ERK signaling, along with epigenetic mechanisms and gene-environment interactions such as oxidative stress, hyperglycemia, and dyslipidemia. Genetic variants in RUNX2 and environmental variables including diet and physical inactivity, amplify its activation, worsening VC and cardiovascular risk. RUNX2 reduces endothelial nitric oxide bioavailability, enhances vascular inflammation, and activates profibrotic signaling in cardiac tissue, promoting vascular dysfunction and myocardial remodeling. Circulating RUNX2 levels and genetic variations exhibit potential as diagnostic and predictive indicators for cardiovascular disease. Severalpharmaceutical agents including metformin, empagliflozin, and statins,   as well as natural substances such green tea polyphenols and green coffee extract, have demonstrated partial modulatory effects on RUNX2 activity. Moreover, genome-editing tools such as CRISPR-Cas9 present future opportunities for selective RUNX2 targeting. Comprehensive understanding of RUNX2 regulation and its interaction with genetic and environmental factors offers novel opportunities for personalized CVD prevention and treatment approaches through lifestyle modification, pharmacotherapy, and gene-based interventions in the future.</dc:description>
	<dc:publisher xml:lang="en">Universitas Brawijaya</dc:publisher>
	<dc:date>2026-04-26</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
	<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
	<dc:format>application/pdf</dc:format>
	<dc:identifier>https://heartscience.ub.ac.id/index.php/heartscience/article/view/20548</dc:identifier>
	<dc:identifier>10.21776/ub.hsj.2026.007.02.5</dc:identifier>
	<dc:source xml:lang="en">Heart Science Journal; Vol. 7 No. 2 (2026): The Evolving Landscape of Heart Failure; 29-35</dc:source>
	<dc:source>2721-9984</dc:source>
	<dc:source>2721-9976</dc:source>
	<dc:source>10.21776/ub.hsj.2026.007.02</dc:source>
	<dc:language>en</dc:language>
	<dc:relation>https://heartscience.ub.ac.id/index.php/heartscience/article/view/20548/576</dc:relation>
	<dc:rights xml:lang="en">Copyright (c) 2026 Anastasia Christine, Mohammad Saifur Rohman, Valerinna Yogibuana</dc:rights>
	<dc:rights xml:lang="en">http://creativecommons.org/licenses/by/4.0</dc:rights>
</oai_dc:dc>