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Advances in Vascular Function, Senescence and Remodeling: A New Direction...
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Advances in Vascular Function, Senescence and Remodeling: A New Direction for Therapeutic Approach to Prevent CVDs

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 August 2026) | Viewed by 1795

Editor

Dr. Gautham Yepuri

E-Mail Website
Guest Editor
Diabetes Research Program, New York University Grossman Medical Center, New York, NY 10012, USA
Interests: cardiovascular diseases; vascular aging; sirtuins; mitochondrial function; heart failure; ischemia reperfusion injury; cell senescence; endothelial biology; induced pluripotent stem cell biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases still remain the leading cause of death worldwide. Sudden cardiac arrest, heart attack, and stroke are on the rise, often leading to unexpected fatalities even before medical attention can be provided. Chronic vascular dysfunction—characterized by sustained vascular inflammatory responses, endothelial cell senescence, remodeling, and vessel collapse or stiffening—can account for cardiovascular and cerebrovascular diseases. A deeper understanding of this area may offer insights into how these events occur. Key challenges we face include the discovery of novel pathways and small molecules that can effectively target them. Current therapeutic approaches have not been successful in preventing mortality or improving clinical outcomes in patients following cardiovascular events. This Special Issue is now accepting articles that focus on novel mechanisms and potential therapeutic strategies to prevent vascular disfunction, cellular senescence, vascular inflammation, and remodeling—processes that may underline the development of cardiovascular diseases.

Dr. Gautham Yepuri
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • vascular dysfunction
  • senescence
  • endothelial cells
  • small molecules
  • anti-aging
  • cardiovascular diseases
  • sudden death

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Published Papers (3 papers)

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Research

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23 pages, 20945 KB  
Article
MCL1 Promotes Endothelial Senescence and Atherosclerosis via Glycolytic Reprogramming-Induced H4K12 Lactylation
by Yang Li, Ling Li, Hongxia Gao, Yakun Gao, Wanying Wu and Longhua Fan
Int. J. Mol. Sci. 2026, 27(16), 7392; https://doi.org/10.3390/ijms27167392 - 18 Aug 2026
Viewed by 455
Abstract
Accumulation of senescent endothelial cells (ECs) accelerates atherosclerosis, yet the molecular orchestrators linking metabolic dysregulation to epigenetic reprogramming during EC senescence remain elusive. Here, we investigated the specific role of Myeloid cell leukemia 1 (MCL1) in endothelial senescence and atherogenesis. Through integrative bioinformatics, [...] Read more.
Accumulation of senescent endothelial cells (ECs) accelerates atherosclerosis, yet the molecular orchestrators linking metabolic dysregulation to epigenetic reprogramming during EC senescence remain elusive. Here, we investigated the specific role of Myeloid cell leukemia 1 (MCL1) in endothelial senescence and atherogenesis. Through integrative bioinformatics, MCL1 was identified as a candidate senescence regulator. MCL1 expression was validated in human carotid atherosclerotic plaques, ApoE−/− mice, and multiple EC senescence models, primarily HRASG12V-induced senescent human umbilical vein endothelial cells (HUVECs). Loss- and gain-of-function assays were performed in HUVECs. Underlying metabolic and epigenetic mechanisms were explored using Seahorse extracellular flux analysis, lactate measurements, Co-IP and CUT&Tag sequencing. In vivo therapeutic potential was evaluated via AAV-mediated MCL1 knockdown in high-fat diet-fed ApoE−/− mice. MCL1 expression was significantly upregulated in atherosclerotic plaques and senescent ECs. Functionally, MCL1 knockdown attenuated senescence markers (SA-β-gal, P21), suppressed the senescence-associated secretory phenotype (SASP), and restored cell proliferation, whereas MCL1 overexpression exacerbated EC senescence. Mechanistically, MCL1 promoted glycolytic reprogramming and intracellular lactate accumulation. This metabolic byproduct served as an epigenetic substrate for histone H4K12 lactylation (H4K12la), which specifically enriched at the CDKN1A (P21) promoter, correlating with its transcription. In vivo, AAV-mediated MCL1 silencing effectively reduced vascular H4K12la levels, alleviated vascular senescence, and substantially constrained atherosclerotic lesion areas. Our findings identify MCL1 as a pivotal regulator of endothelial senescence and atherosclerosis, operating through a metabolic-\–epigenetic mechanism involving glycolytic reprogramming, lactate accumulation, and H4K12la-associated P21 upregulation. These findings suggest that targeting the MCL1-associated pathway may represent a potential therapeutic strategy for atherosclerosis. Full article
(This article belongs to the Special Issue Advances in Vascular Function, Senescence and Remodeling: A New Direction for Therapeutic Approach to Prevent CVDs)
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35 pages, 13909 KB  
Article
Exercise Modulates miR-276a/nej Expression and Function in the Drosophila Heart: A Possible Contribution of the Fat Body
by Qin Yi, Chao Tang, Qiufang Li, Meng Ding, Zhihao Pan, Zhengwen Yu, Xu Ping, Wenzhi Gu, Yuepeng Li, Ni Ding, Wenqing Huang, Jin Dai, Xinrui Xu, Shiyi He and Lan Zheng
Int. J. Mol. Sci. 2026, 27(15), 6640; https://doi.org/10.3390/ijms27156640 - 25 Jul 2026
Viewed by 346
Abstract
Cardiac rhythm and pumping function are essential outputs of cardiac homeostasis and depend on precise molecular regulation. The histone acetyltransferases CBP/p300 have been implicated in cardiac remodeling and functional regulation. nej, the Drosophila homolog of CBP/p300, may therefore represent an important regulator of [...] Read more.
Cardiac rhythm and pumping function are essential outputs of cardiac homeostasis and depend on precise molecular regulation. The histone acetyltransferases CBP/p300 have been implicated in cardiac remodeling and functional regulation. nej, the Drosophila homolog of CBP/p300, may therefore represent an important regulator of cardiac function. However, the relationship between miR-276a and nej in the heart, as well as the potential involvement of the fat body in this regulatory relationship, remains unclear. Using Drosophila as a model, we first examined the effects of cardiac-specific nej overexpression and knockdown on cardiac function and tested the interaction between miR-276a and the nej 3′ untranslated region using a dual-luciferase reporter assay. We subsequently manipulated miR-276a using Hand-Gal4 and Cg-Gal4 and assessed miR-276a and nej expression in cardiac samples, cardiac function, and climbing ability. Finally, we investigated the effects of an exercise intervention on cardiac miR-276a/nej expression and functional outcomes. Both cardiac-specific overexpression and knockdown of nej impaired cardiac rhythm, reduced pumping function, and decreased climbing ability. The reporter assay supported a functional interaction between miR-276a and the nej 3′ untranslated region, while cardiac-specific miR-276a manipulation was accompanied by inverse changes in nej mRNA expression and by cardiac and climbing abnormalities. Cg-Gal4-mediated miR-276a upregulation or downregulation was associated with altered miR-276a and nej expression in cardiac samples and with cardiac and climbing impairments. Exercise improved cardiac and climbing ability in both cardiac miR-276a knockdown and overexpression groups. It increased cardiac miR-276a expression and decreased nej expression in the cardiac knockdown group but did not significantly alter either transcript in the cardiac overexpression group. Exercise also improved cardiac function in both Cg-Gal4-mediated miR-276a knockdown and overexpression groups. In the Cg-Gal4-mediated knockdown group, this improvement was accompanied by increased miR-276a and decreased nej expression in cardiac samples. These findings indicate that exercise modulates cardiac function and miR-276a/nej expression in a context-dependent manner and suggests a possible contribution of the fat body. Full article
(This article belongs to the Special Issue Advances in Vascular Function, Senescence and Remodeling: A New Direction for Therapeutic Approach to Prevent CVDs)
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Review

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18 pages, 1462 KB  
Review
Immunologically Adaptive Endovascular Devices: Integrating Thrombo-Inflammation, Biomaterials Design, and Artificial Intelligence for Precision Cardiovascular Intervention
by Rasit Dinc and Nurittin Ardic
Int. J. Mol. Sci. 2026, 27(8), 3493; https://doi.org/10.3390/ijms27083493 - 14 Apr 2026
Cited by 1 | Viewed by 630
Abstract
Endovascular therapies have transformed cardiovascular medicine, yet restenosis, thrombosis, and device failure remain common and poorly predictable complications. Increasing evidence suggests that immunothrombotic processes critically shape vascular recovery after device implantation. This includes neutrophil extracellular trap (NET) formation, innate immune polarization, and endothelial [...] Read more.
Endovascular therapies have transformed cardiovascular medicine, yet restenosis, thrombosis, and device failure remain common and poorly predictable complications. Increasing evidence suggests that immunothrombotic processes critically shape vascular recovery after device implantation. This includes neutrophil extracellular trap (NET) formation, innate immune polarization, and endothelial damage responses. Concurrently, advances in artificial intelligence (AI) are increasingly enabling continuous multimodal monitoring and adaptive clinical decision-making throughout the medical device life cycle. Here, we propose the concept of immunologically adaptive endovascular devices: a closed-loop paradigm in which patient immune status informs device selection, device–tissue interactions are interpreted via mechanistic biomarkers, and real-world monitoring dynamically updates risk and management. The study introduces (i) an immune–device interaction phenotype taxonomy linking device design features to measurable thrombo-inflammatory trajectories, (ii) a mechanistic framework defining interface signaling processes that enhance or resolve NET-driven responses, (iii) a minimum evidence model encompassing preclinical testing, clinical validation, and post-market surveillance, and (iv) a reference AI architecture for risk prediction, drift detection, and safety monitoring. This study also outlined testable predictions and a translational roadmap toward precision endovascular intervention and next-generation adaptive cardiovascular devices. Full article
(This article belongs to the Special Issue Advances in Vascular Function, Senescence and Remodeling: A New Direction for Therapeutic Approach to Prevent CVDs)
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