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Unravelling the Intricate Link Between Microvascular Dysfunction and Cardiovascular Disease

Special Issue Editor


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Guest Editor
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary
Interests: microvascular dysfunction; cardiovascular diseases; endothelial dysfunction; oxidative stress

Special Issue Information

Dear Colleagues,

Microvascular dysfunction is a key factor in the pathogenesis of cardiovascular diseases (CVDs), contributing to heart failure, major adverse cardiovascular events, and increased cardiovascular mortality. The microvasculature, composed of small resistance arteries, arterioles, capillaries, and venules, plays an essential role in regulating perfusion, fluid and solute exchange, haemostasis, inflammation, and angiogenesis. Dysfunction in these vessels, characterized by structural and/or functional alterations, leads to impaired tissue perfusion and target organ damage.

Recent advances in research have unveiled the molecular mechanisms underlying microvascular dysfunction, highlighting the pivotal roles of endothelial dysfunction, oxidative stress, reduced nitric oxide (NO) bioavailability, VEGF dysregulation, and endothelin-1 overactivity. These processes are further implicated in conditions such as diabetes, hypertensive disorders of pregnancy, chronic kidney disease, rheumatoid arthritis, and aortic valve stenosis. Notably, microvascular dysfunction often precedes the onset of diastolic dysfunction and heart failure with preserved ejection fraction (HFpEF).

Building on these insights, innovative pharmacological strategies to restore microvascular health are highly needed. Potential therapies can include NO donors, endothelin receptor antagonists, VEGF modulators, mitochondrial-targeted agents, and other new therapies. Anti-inflammatory treatments and advanced glycation end-product (AGE) inhibitors are also being investigated to mitigate oxidative stress and chronic inflammation. These advances (including but not limited to them) emphasize the potential of mechanism-specific interventions to improve microvascular function, prevent disease progression, and enhance cardiovascular outcomes.

The understanding of the molecular basis of microvascular dysfunction has paved the way for promising and innovative pharmacological therapeutic avenues. Targeting these pathways offers significant opportunities with which to address cardiovascular diseases at their roots, making microcirculation a critical focus for future research and treatment strategies.

This Special Issue focuses on the latest molecular insights into microvascular dysfunction and its pivotal role in cardiovascular pathogenesis. It aims to achieve the following:

  • Explore the molecular mechanisms driving microvascular dysfunction.
  • Highlight its implications in various systemic conditions, including diabetes and chronic kidney disease.
  • Novel and innovative therapeutic strategies, such as NO donors, VEGF modulators, endothelin receptor antagonists, mitochondrial-targeted agents, anti-inflammatory therapies, AGE inhibitors, and other new therapies.
  • Discuss innovative approaches for restoring microvascular health and preventing disease progression.
  • Foster multidisciplinary research to identify mechanism-specific interventions that improve cardiovascular outcomes.

This Special Issue serves as a platform with which to integrate fundamental discoveries with translational research, emphasizing microcirculation as a critical target for future cardiovascular therapies.

Dr. Róbert Pórszász
Guest Editor

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Keywords

  • microvascular dysfunction
  • cardiovascular pathogenesis
  • endothelial dysfunction
  • oxidative stress
  • nitric oxide bioavailability
  • VEGF dysregulation
  • endothelin-1 overactivity
  • heart failure with preserved ejection fraction (HFpEF)
  • pharmacological interventions
  • microcirculation-targeted therapies

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Published Papers (1 paper)

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Review

27 pages, 2385 KiB  
Review
Butyrate Produced by Gut Microbiota Regulates Atherosclerosis: A Narrative Review of the Latest Findings
by Leon M. T. Dicks
Int. J. Mol. Sci. 2025, 26(14), 6744; https://doi.org/10.3390/ijms26146744 - 14 Jul 2025
Viewed by 531
Abstract
Atherosclerosis (AS), a progressive inflammatory disease of coronary arteries, the aorta, and the internal carotid artery, is considered one of the main contributors to cardiovascular disorders. Blood flow is restricted by accumulating lipid-rich macrophages (foam cells), calcium, fibrin, and cellular debris into plaques [...] Read more.
Atherosclerosis (AS), a progressive inflammatory disease of coronary arteries, the aorta, and the internal carotid artery, is considered one of the main contributors to cardiovascular disorders. Blood flow is restricted by accumulating lipid-rich macrophages (foam cells), calcium, fibrin, and cellular debris into plaques on the intima of arterial walls. Butyrate maintains gut barrier integrity and modulates immune responses. Butyrate regulates G-protein-coupled receptor (GPCR) signaling and activates nuclear factor kappa-B (NF-κB), activator protein-1 (AP-1), and interferon regulatory factors (IFRs) involved in the production of proinflammatory cytokines. Depending on the inflammatory stimuli, butyrate may also inactivate NF-κB, resulting in the suppression of proinflammatory cytokines and the stimulation of anti-inflammatory cytokines. Butyrate modulates mitogen-activated protein kinase (MAPK) to promote or suppress macrophage inflammation, muscle cell growth, apoptosis, and the uptake of oxidized low-density lipoprotein (ox-LDL) in macrophages. Activation of the peroxisome proliferator-activated receptor γ (PPARγ) pathway plays a role in lipid metabolism, inflammation, and cell differentiation. Butyrate inhibits interferon γ (IFN-γ) signaling and suppresses NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) involved in inflammation and scar tissue formation. The dual role of butyrate in AS is discussed by addressing the interactions between butyrate, intestinal epithelial cells (IECs), endothelial cells (ECs) of the main arteries, and immune cells. Signals generated from these interactions may be applied in the diagnosis and intervention of AS. Reporters to detect early AS is suggested. This narrative review covers the most recent findings published in PubMed and Crossref databases. Full article
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