Microcirculation最新文献

Blood vessels form an intricate network of dynamic conduits responsible for delivering blood throughout the body. Consequently, the structural and functional integrity of blood vessels is critical for optimal circulation and tissue function. Vascular reactivity is an essential physiological process by which blood vessels dynamically adjust their diameter in response to various stimuli. This adaptive process ensures that blood flow meets tissue-specific metabolic demands. Vascular reactivity is also essential for controlling blood pressure, as changes in the radius of resistance vessels dramatically affect peripheral vascular resistance.

Vascular reactivity is governed by sophisticated signaling cascades within and between various cell types constituting the vascular wall (smooth muscle cells, pericytes, and endothelial cells), perivascular adipose tissue that surrounds most blood vessels, and many types of additional extravascular cells. These diverse signaling cascades give rise to regional heterogeneity in vascular responses, leading to distinctive reactivity patterns tailored to the physiological role of individual vessel segments. An array of different hormones and circulating factors can also influence vascular reactivity, and considering sex as a biological variable has provided valuable insights into the mechanisms underlying vascular function.

The importance of vascular reactivity extends beyond basic vessel physiology, as its altered function underpins physiological vascular adaptation during pregnancy and numerous pathological conditions such as hypertension, heart failure, and stroke. Thus, elucidating the intricate mechanisms, functional implications, and adaptive responses, as well as developing new tools and approaches to better study vascular reactivity, is paramount for advancing cardiovascular research and the development of new treatment strategies.

In this Special Topics Issue (STI), we present a curated collection of reviews and original studies that expand our current knowledge of mechanisms and functional implications of vascular reactivity in health, physiological adaptation, and disease states. The reader will also find studies introducing innovative methodological approaches and analytical techniques for examining vascular reactivity, creating opportunities to advance future research endeavors in vascular biology.

This STI begins with a review by Li and colleagues [1] dissecting the role of ion channels in vascular cells and their contributions to vascular hyporesponsiveness during shock. The authors examine how structural and functional alterations in various ion channels (e.g., K⁺, Ca²⁺, and Na⁺ channels) contribute to altered vascular reactivity during shock and how this new mechanistic insight could be exploited for the development of new therapies to treat shock-induced vascular complications.

Following the ion channel theme, Mbiakop and J

Coronary microvascular disease (CMVD) affects the coronary pre-arterioles, arterioles, and capillaries and can lead to blood supply–demand mismatch and cardiac ischemia. CMVD can present clinically as ischemia or myocardial infarction with no obstructive coronary arteries (INOCA or MINOCA, respectively). Currently, therapeutic options for CMVD are limited, and there are no targeted therapies. Genetic studies have emerged as an important tool to gain rapid insights into the molecular mechanisms of human diseases. For example, coronary artery disease (CAD) genome-wide association studies (GWAS) have enrolled hundreds of thousands of patients and have identified > 320 loci, elucidating CAD pathogenic pathways and helping to identify therapeutic targets. Here, we review the current landscape of genetic studies of CMVD, consisting mostly of genotype-first approaches. We then present the hypothesis that CAD GWAS have enrolled heterogenous populations and may be better characterized as ischemic heart disease (IHD) GWAS. We discuss how several of the genetic loci currently associated with CAD may be involved in the pathogenesis of CMVD. Genetic studies could help accelerate progress in understanding CMVD pathophysiology and identifying putative therapeutic targets. Larger phenotype-first genomic studies into CMVD with adequate sex and ancestry representation are needed. Given the extensive CAD genetic and functional validation data, future research should leverage these loci as springboards for CMVD genomic research.