Physiology is a wide spanning discipline, and it is interesting to follow its journey into the unknown in different organs, and with ever more sophisticated methods. This research is reflected by high quality publications in physiological journals. Have a look!
The results of this research as well as of comparative physiology and mathematical modelling, provide ever growing insight into the body’s functions, mechanisms of disease and new therapies, including gene therapy and development of vaccines. The close interaction between basic physiological research and clinical work, has improved human health and life span and holds even more promises for the future.
A most interesting aspect of current physiology is that, unlike in past centuries, novel models and techniques have reduced or replaced the need to destroy or dissect organs and tissues to improve understanding of function. Now we can learn from growing cells and stimulating them to form tissues and even “organs”. It has become almost routine for physiologists to manipulate gene expression to study function in the intact animal. We are obtaining novel and unique insights into the principles of self-organisation of cells and their mutual interactions. Exciting times, indeed!
Physiology is a wide spanning discipline, and it is interesting to follow its journey into the unknown in different organs, and with ever more sophisticated methods. This research is reflected by high quality publications in physiological journals. Have a look!
Kelsey C. Muir et al.
NEW & NOTEWORTHY In a clinically relevant swine model of chronic ischemic cardiomyopathy, oral semaglutide improved ventricular performance, likely through enhanced coronary collateralization. This benefit holds particular promise for patients with obesity and type 2 diabetes—populations already eligible for GLP-1 analog therapy. These findings support the initiation of randomized clinical trials of early GLP-1R agonist use at the time of CAD diagnosis to assess long-term outcomes and potential incorporation into standard ischemic heart disease management.
Burook Misganaw et al.
NEW & NOTEWORTHY This study investigated the first multiomics data for association with tolerance to central hypovolemia in humans. Analyzing gene expression, proteins, and genetic variants in individuals with high and low tolerance to simulated hemorrhage, the findings show that severe blood loss causes widespread transcriptional changes, including the activation of innate immune system pathways and inhibition of gas transport processes. This research can help identify molecular factors that influence individuals’ tolerance levels for progressive blood loss.
et al. (invited Review)
Ancient DNA and human physiology (invited review)
From the abstract: Ancient DNA has the potential to link sequence variation to physiological function within their temporal and environmental contexts. In this review, we summarize illustrative case studies from aDNA research spanning complex traits, dietary adaptations, and responses to pathogens and other environmental changes, showing how human biology has evolved under multiple selective pressures through time. These dated signals help triage experimental work and expose mechanisms that are rare or absent in living cohorts. While some challenges remain, such as geographic and temporal sampling disparities, technical limitations, and genotype-phenotype uncertainties, rapid methodological progress and stronger ethical frameworks are expanding what can be inferred, making aDNA a promising tool for refining physiological pathways, their timing, and their drivers.
Much more can be found in this month’s selection of articles from APS journals!
These new and engaging video feature from The Journal of Physiology aims to deliver short and informative research snapshots directly from the authors of research papers selected by the Editors of the journal!
The latest topic relates to an article published by Yoshioka D. and Okamura Y in PNAS
From the abstract : KCNQ2/3, a major voltage-gated potassium channel at the axon initial segment (AIS), plays a crucial role in controlling neuronal excitability. While the functionality of KCNQ2/3 is regulated by conformational changes from voltage sensing, the AIS localization of KCNQ2/3 is regulated by ankyrinG (ankG). However, the potential coupling between the mechanisms governing channel functionality and trafficking remains unresolved. Single-molecule imaging reveals that reduced KCNQ3 functionality alters the entire trafficking pathway, including exo/endocytosis and lateral diffusion, reducing AIS localization of KCNQ2/3. Furthermore, a live-cell assay to quantify the interactions between full-length KCNQ3 and ankG, demonstrated that the active conformation of KCNQ3 is essential for the stable ankG binding. Our findings establish a mechanistic basis for the integration of KCNQ2/3 gating and trafficking in regulating neuronal excitability
PSJ celebrated its 100th anniversary in 2023. On this occasion the Journal of Physiology compiled a collection of some of the most influential research published by Japanese authors in this journal. Have a closer look here!
DPG’s latest paper of the month (Karen Lahme et al) was recently published in Cell.
From the abstract: Chronic kidney disease affects 1 in 10 people worldwide, with damage to specialized blood filter cells of the kidney, called podocytes, playing a critical role. In membranous nephropathy (MN), a major cause of nephrotic syndrome, circulating autoantibodies attack proteins on podocyte foot processes (FPs), damaging the kidney’s filtration barrier. This study shows that these autoantibodies trigger the formation of antigen-autoantibody aggregates on the podocyte FP plasma membrane. These aggregates bud off as stalked vesicles, termed autoimmunoglobulin-triggered extracellular vesicles (AIT-EVs), which are released into the urine. AIT-EVs carry disease-causing autoantibodies, their target antigens, essential FP proteins, and disease-associated stressors representing a mechanism for removing immune complexes (ICs) and waste. However, their excessive release leads to FP effacement and podocyte dysfunction. In MN patients, urinary AIT-EVs correspond to glomerular urinary-space aggregates. Enriching AIT-EVs enables detection and monitoring of pathogenic autoantibodies, suggesting a non-invasive approach for autoimmune kidney disease diagnosis and therapy.