109 papers
Physiology explores how living systems function, from the microscopic signals inside a single cell to the complex rhythms of an entire organism. This field seeks to understand the mechanical, physical, and biochemical processes that keep life moving, offering crucial insights into health, disease, and the body's remarkable ability to adapt.
On Gist.Science, we process every new preprint in this category from bioRxiv to make these rapid discoveries accessible to everyone. For each study, we provide both a clear, plain-language explanation and a detailed technical summary, ensuring that whether you are a curious student or a seasoned researcher, you can grasp the latest findings without getting lost in jargon.
The papers listed below represent the newest physiological research recently shared on bioRxiv, ready for you to explore.
This study demonstrates that the extracellular matrix retains a "memory" of metabolic dysfunction-associated steatohepatitis (MASH) that persists after decellularization, actively promoting steatosis, fibrosis, and metabolic dysfunction in both in vitro and in vivo settings, thereby confirming that diseased ECM can drive disease progression even when repopulated with healthy cells.
This study demonstrates that above-chance decoding of emotion from single-trial EEG during imagined vocalisation is largely driven by involuntary facial muscle activity, particularly for happiness, rather than purely neural speech signals.
This study demonstrates that chronic treatment with the α1A-adrenergic agonist A61603 reverses right ventricular failure in a mouse model by restoring mitochondrial function, specifically improving oxygen consumption and ATP levels.
This study proposes a theoretical framework demonstrating that sarcomere length dynamics during the isovolumic phases, regulated by the balance between ventricular volume and contraction force rather than volume alone, mechanically modulate contractile force to shorten isovolumic relaxation time and enhance hemodynamic efficiency.
This study demonstrates that a specific high-fat, high-cholesterol, and fructose-supplemented diet successfully induces obesity and MASLD in both male and female mice, but progression to MASH with fibrosis occurs exclusively in males through a hepatocyte PPARγ-dependent mechanism involving the downregulation of methionine metabolism.
This study utilizes multi-omic profiling to demonstrate that small and large plasma extracellular vesicles in early pregnancy possess distinct yet complementary molecular signatures reflecting placental, metabolic, and structural adaptations, thereby establishing a foundational framework for linking these vesicle subtypes to pregnancy outcomes.
This study demonstrates that Angiotensin II exacerbates vascular injury by amplifying CCL5/CCR5 signaling, which drives mitochondrial dysfunction and oxidative stress in vascular smooth muscle cells, thereby promoting vascular inflammation and impairment.
This paper argues that *eat-2* mutants in *C. elegans* are an unreliable model for dietary restriction studies because their extended lifespan is primarily caused by reduced susceptibility to bacterial infection rather than a genuine dietary restriction effect.
This study demonstrates that TUDCA treatment restores vascular and perivascular adipose tissue function in male mice subjected to post-weaning protein restriction by attenuating endoplasmic reticulum stress, fibrosis, and associated molecular dysregulation.
This study demonstrates that chronically elevated FGF23 levels drive sustained renal ERK signaling and inflammatory responses in chronic kidney disease, which can be effectively mitigated by C-terminal FGF23 (cFGF23) gene therapy.