Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
6.0
3.4
Journals
Life
Special Issues
Regulation of Cerebrovascular Resistance in Health and Disease: From Molecules...
share announcement

Regulation of Cerebrovascular Resistance in Health and Disease: From Molecules to Humans

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: 13 February 2026 | Viewed by 4572

Special Issue Editor

Dr. Akos Koller

E-Mail
Guest Editor
1. Institute of Translational Medicine, HUN-REN-SE, Cerebrovascular and Neurocognitive Disease Research Group, Semmelweis University, Budapest, Hungary
2. Research Center for Sport Physiology, Hungarian University of Sports Science, Budapest, Hungary
3. Department of Physiology, New York Medical College, Valhalla, NY, USA
Interests: regulation of cerebral blood flow in heath and diseased conditions

Special Issue Information

Dear Colleagues,

Optimal cerebrovascular perfusion is vital for maintaining healthy brain function. This complete task is achieved by different and appropriate mechanisms regulating the resistance of various extracranial and intracranial vessels, such as arteries, arterioles, and even venules.

One of the specific attributes of cerebral circulation is its well-developed autoregulation. This tight control of cerebral blood flow (CBF) is crucial to maintaining a relatively constant blood supply of the brain, as well as intracranial blood volume, and at the same time to comply with the limited space available in the skull.

Thus, small intracranial cerebral arteries have a well-developed constrictor function. On the other hand, this limitation does not affect extracranial arteries, allowing them to dilate freely, thus providing increased blood flow to the brain. Hemodynamic forces play an important role in the autoregulation of CBF, as previous studies have established that it is achieved by pressure- and flow-sensitive vasomotor mechanisms. In addition to these, other cellular, metabolic, and neural factors also play important roles in enabling brain tissues to control cerebrovascular resistance and thus blood supply, mechanisms collectively called neurovascular coupling.

In diseased conditions, such as hypertension, diabetes, pre-eclampsia, traumatic brain injury, aging, etc., these mechanisms can become impaired, leading to stroke, micro-bleeding, edema, Alzheimer-like dementia, and so on.

Many of the underlying molecular and functional pathomechanisms are still unresolved; thus, both basic and clinical research are needed to elucidate them.

We invite the submission of manuscripts to this Special Issue that will contribute to improving our understanding of the mechanisms responsible for the appropriate supply and autoregulation of cerebral blood flow and reveal the pathomechanisms responsible for disease relate conditions fostering the development of appropriate preventions and therapies.

Dr. Akos Koller
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 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • cerebral blood flow
  • hemodynamic forces
  • cerebrovascular resistance
  • endothelium
  • smooth muscle
  • arachidonic acid metabolites
  • reactive oxygen species
  • molecular mediators
  • protein and mRNA expressions
  • brain disease conditions
  • transcranial Doppler measurement
  • EEG
  • lifestyle

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (5 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

11 pages, 1294 KB  
Article
Cerebral Resistance Artery Histological Remodeling After Training—Sex Differences
by Tobias Hainzl, György L. Nádasy, Emese Róza Márka, Kamilla Nagy, Réka Kollarics, Anna-Mária Tőkés, Attila Oláh, Tamás Radovits, Béla Merkely, Nándor Ács, Szabolcs Várbíró, Attila Jósvai and Marianna Török
Life 2025, 15(8), 1304; https://doi.org/10.3390/life15081304 - 17 Aug 2025
Viewed by 731
Abstract
Background: Chronic exercise has been linked to positive effects on cognitive function and brain health. The aim of our study was to investigate how exercise affects cerebral resistance artery morphology, with an underlying focus on potential sex differences. Methods: Wistar rats [...] Read more.
Background: Chronic exercise has been linked to positive effects on cognitive function and brain health. The aim of our study was to investigate how exercise affects cerebral resistance artery morphology, with an underlying focus on potential sex differences. Methods: Wistar rats were divided into male exercising (M.Ex; n = 6), female exercising (F.Ex; n = 5), male sedentary (M.Sed; n = 5), and female sedentary (F.Sed; n = 5) groups. After a 12-week swimming program, histological examinations of the intracerebral and pial arterioles were performed. SMA-DAB (smooth muscle actin) and resorcin-fuchsin (elastica) stained brain coronal sections were used for quantitative colorimetric analysis. Results: Investigating the effect of exercise, we found that in both pial and intracerebral arterioles, the elastic fiber density increased in both female and male exercising animals compared to the sedentary groups (p < 0.05 (M.Sed vs. M.Ex); p < 0.0001 (F.Sed vs. F.Ex)). As sex differences, we found that in female animals’ pial arterioles, the density of elastic fiber was increased compared to the male exercising group (p < 0.001 (M.Ex vs. F.Ex)). In pial arterioles, the smooth muscle density was higher in the male sedentary animals (p < 0.01 (M.Sed vs. F.Sed)); in intracerebral arterioles, the smooth muscle density increased with exercise in the male animals as well (p < 0.0001 (M.Ex vs. F.Ex)). Conclusions: Our results demonstrate that the increase in vascular elasticity is more pronounced overall in female animals. Full article
(This article belongs to the Special Issue Regulation of Cerebrovascular Resistance in Health and Disease: From Molecules to Humans)
►▼ Show Figures

Figure 1

22 pages, 1715 KB  
Article
Differential Gene and Protein Expressions Responsible for Vasomotor Signaling Provide Mechanistic Bases for the Opposite Flow-Induced Responses of Pre- and Post-Circle of Willis Arteries
by Zoltan Nemeth, Krisztian Eros, Gyongyi Munkacsy and Akos Koller
Life 2025, 15(6), 856; https://doi.org/10.3390/life15060856 - 26 May 2025
Viewed by 845
Abstract
Increases in flow elicit dilations in the basilar artery (BA) supplied by the posterior cerebral circulation (PCC), and ensuring efficient blood supply to the circle of Willis in which blood flow and pressure can distribute and equalize, and thus provide the appropriate supply [...] Read more.
Increases in flow elicit dilations in the basilar artery (BA) supplied by the posterior cerebral circulation (PCC), and ensuring efficient blood supply to the circle of Willis in which blood flow and pressure can distribute and equalize, and thus provide the appropriate supply for the daughter branches to reach certain brain areas. In contrast, increases in flow elicit constrictions in the middle cerebral artery (MCA), supplied by the anterior cerebral circulation (ACC) and regulating the blood pressure and flow in distal cerebral circulation. Mediators of flow-dependent responses include arachidonic acid (AA) metabolites and nitric oxide (NO). We hypothesized that mediators of flow-dependent responses are differentially expressed in cerebral arteries of the PCC (CAPCC) and ACC (CAACC). The expressions of key enzymes of the AA pathway—cyclooxygenases (COX1/COX2), cytochrome P450 hydroxylases (Cyp450), thromboxane synthase (TXAS), thromboxane A2 (TP) receptor, prostacyclin synthase (PGIS), prostacyclin (IP) receptor (IP); neuronal nitric oxide synthase (nNOS), and endothelial nitric oxide synthase (eNOS)—in the BA and MCA from rats (n = 20) were determined by western blotting. Transcriptome analysis in CAPCC and CAACC from rats (n = 25) was assessed by RNA sequencing. In BA compared to MCA, COX1/2 and Cyp450 protein expressions were lower, PGIS was higher, TXAS and nNOS/eNOS were similar, TP receptors were lower, and IP receptors were higher. Gene expressions of vasodilator canonical pathways were higher in CAPCC; vasoconstriction canonical pathways were higher in CAACC. Mediators of flow-dependent vasomotor signaling are differentially expressed in cerebral arteries of the posterior and anterior circulation, corresponding to their vasomotor function. Full article
(This article belongs to the Special Issue Regulation of Cerebrovascular Resistance in Health and Disease: From Molecules to Humans)
►▼ Show Figures

Figure 1

Review

Jump to: Research

29 pages, 1081 KB  
Review
Intracerebral Hemorrhage in Aging: Pathophysiology, Clinical Challenges, and Future Directions
by Esra Zhubi, Andrea Lehoczki, Peter Toth, Dominika Lendvai-Emmert, Levente Szalardy and Bence Gunda
Life 2025, 15(10), 1569; https://doi.org/10.3390/life15101569 - 8 Oct 2025
Viewed by 712
Abstract
Spontaneous intracerebral hemorrhage (ICH) is a devastating form of stroke, disproportionately affecting older adults and is associated with high rates of mortality, functional dependence, and long-term cognitive decline. Aging profoundly alters the structure and function of the cerebral vasculature, predisposing the brain to [...] Read more.
Spontaneous intracerebral hemorrhage (ICH) is a devastating form of stroke, disproportionately affecting older adults and is associated with high rates of mortality, functional dependence, and long-term cognitive decline. Aging profoundly alters the structure and function of the cerebral vasculature, predisposing the brain to both covert hemorrhage and the development of cerebral microbleeds (CMBs), small, often subclinical lesions that share common pathophysiological mechanisms with ICH. These mechanisms include endothelial dysfunction, impaired cerebral autoregulation, blood–brain barrier breakdown, vascular senescence, and chronic inflammation. Systemic factors such as age-related insulin-like growth factor 1 (IGF-1) deficiency further exacerbate microvascular vulnerability. CMBs and ICH represent distinct yet interconnected manifestations along a continuum of hemorrhagic small vessel disease, with growing recognition of their contribution to vascular cognitive impairment and dementia (VCID). Despite their increasing burden, older adults remain underrepresented in clinical trials, and few therapeutic approaches specifically target aging-related mechanisms. This review synthesizes current knowledge on the cellular, molecular, and systemic drivers of ICH and CMBs in aging, highlights diagnostic and therapeutic challenges, and outlines opportunities for age-sensitive prevention and individualized care strategies. Full article
(This article belongs to the Special Issue Regulation of Cerebrovascular Resistance in Health and Disease: From Molecules to Humans)
►▼ Show Figures

Figure 1

23 pages, 1010 KB  
Review
Cerebral Vascular Disturbances Following Traumatic Brain Injury: Pathophysiology, Diagnosis, and Therapeutic Perspectives—A Narrative Review
by Nicoleta-Larisa Serban, Gheorghe Ungureanu, Ioan Stefan Florian and Daniela Ionescu
Life 2025, 15(9), 1470; https://doi.org/10.3390/life15091470 - 18 Sep 2025
Viewed by 884
Abstract
Traumatic brain injury (TBI) is a major global health concern and a leading cause of long-term disability and mortality. While the primary mechanical insult is often the focus of acute care, secondary injury mechanisms—particularly cerebrovascular dysfunction—play a critical role in ongoing neural damage [...] Read more.
Traumatic brain injury (TBI) is a major global health concern and a leading cause of long-term disability and mortality. While the primary mechanical insult is often the focus of acute care, secondary injury mechanisms—particularly cerebrovascular dysfunction—play a critical role in ongoing neural damage and poor outcomes. Increasing research highlights the role of neurovascular changes in TBI pathophysiology. This narrative review compiles evidence from the past decade on mechanisms, diagnostic methods, and treatments related to cerebrovascular dysfunction after TBI. A structured search of PubMed and Embase identified relevant clinical and preclinical studies. Key mechanisms include blood–brain barrier disruption, impaired cerebral autoregulation, microthrombosis, and oxidative stress. Diagnostic tools discussed include perfusion imaging, cerebrovascular reactivity testing, and blood-based biomarkers of vascular injury. Therapeutic strategies targeting the neurovascular unit are categorized by mechanism: anti-inflammatory agents (e.g., celecoxib, minocycline), mitochondrial protectors (e.g., Tanshinone IIA), and vasomodulators (e.g., sildenafil). We propose an integrated therapeutic approach for a multimodal treatment plan that integrates these interventions. The findings emphasize the importance of patient-specific vascular therapies to reduce secondary ischemic injury and enhance neurological recovery. Although promising preclinical data exist, clinical application remains limited. More well-designed trials are needed to confirm the safety and effectiveness of emerging therapies. Full article
(This article belongs to the Special Issue Regulation of Cerebrovascular Resistance in Health and Disease: From Molecules to Humans)
►▼ Show Figures

Figure 1

20 pages, 1126 KB  
Review
Review of the Role of TRAF7 in Brain Endothelial Integrity and Cerebrovascular Aging
by Jennifer Ihuoma, Sherwin Tavakol, Sharon Negri, Cade Ballard, Khanh Phan, Albert Orock, Zeke Reyff, Madison Milan, Eva Troyano-Rodriguez, Rakesh Rudraboina, Anna Csiszar, Anthony C. Johnson, Ian F. Dunn and Stefano Tarantini
Life 2025, 15(8), 1280; https://doi.org/10.3390/life15081280 - 12 Aug 2025
Viewed by 975
Abstract
Tumor necrosis factor (TNF) receptor-associated factor 7 (TRAF7) is a signal transducer in the TNF receptor superfamily. TRAF7 is unique among its superfamily in that it does not contain a TRAF-C domain but does contain WD-40 domains. TRAF7 interacts with mitogen-activated protein kinases [...] Read more.
Tumor necrosis factor (TNF) receptor-associated factor 7 (TRAF7) is a signal transducer in the TNF receptor superfamily. TRAF7 is unique among its superfamily in that it does not contain a TRAF-C domain but does contain WD-40 domains. TRAF7 interacts with mitogen-activated protein kinases (MAPK), which are known regulators of inflammation and shear stress response. Notably, these molecular interactions have profound implications for the function of brain endothelial cells (ECs), which are pivotal for sustaining the integrity of the blood–brain barrier (BBB), orchestrating neurovascular coupling (NVC), and modulating the vascular architecture. By directly influencing MAPK signaling pathways, particularly the shear stress-responsive MAPK kinase kinase 3 (MEKK3)–MAPK kinase 5 (MEK5)–extracellular-regulated protein kinase 5 (ERK5) cascade, TRAF7 contributes to vascular homeostasis, as exemplified by its role in phosphorylating ERK5. Such molecular events underpin the capacity of brain ECs to regulate substance exchange, adjust blood flow in response to neural activity, and maintain efficient cerebral perfusion, all of which are essential for preserving brain health and cognitive performance. By synthesizing the current evidence regarding TRAF7’s molecular functions and its impact on brain endothelial integrity, cerebrovascular aging, and exploring implications for therapeutic strategies targeting vascular dysfunction in the aging brain, this review fills a crucial gap in the literature. Given the limited number of original studies directly addressing these contexts, the review will integrate broader insights from related literature to provide a foundational overview for future research in this developing field. The culmination of this literature will provide a rationale for the development of novel TRAF7-targeted therapies to restore vascular integrity in the context of aging, which could maintain cognitive health. Although TRAF7 has been implicated in regulating endothelial permeability during inflammation, its precise functions in brain ECs and the subsequent effects on cerebrovascular structure and cognitive function remain to be fully elucidated. Full article
(This article belongs to the Special Issue Regulation of Cerebrovascular Resistance in Health and Disease: From Molecules to Humans)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop