M. Regnier

Hypertrophic cardiomyopathy mutations Y115H and E497D disrupt the folded-back state of human beta-cardiac myosin allosterically

This study investigates how HCM mutations Y115H and E497D disrupt the folded-back state of human beta-cardiac myosin, leading to hypercontractility by destabilizing the OFF-state.

Far-red and sensitive sensor for monitoring real-time H2O2 dynamics with subcellular resolution and inmulti-parametric imaging applications.

This paper introduces a new fluorescent sensor, oROS-HT, for real-time H2O2 monitoring with subcellular resolution and multi-parametric imaging capabilities.

p110alpha-dependent hepatocyte signaling is critical for liver gene expression and its rewiring in MASLD

This study investigates the role of p110alpha in hepatocyte signaling, showing its critical impact on liver gene expression and its rewiring in MASLD.

Late-life Rapamycin Treatment Enhances Cardiomyocyte Relaxation Kinetics and Reduces Myocardial Stiffness

This study shows that late-life rapamycin treatment improves cardiomyocyte relaxation and reduces myocardial stiffness in aged mice, reversing diastolic dysfunction.

MBNL1 regulates programmed postnatal switching between regenerative and differentiated cardiac states.

This study identifies MBNL1 as a regulator of cardiac cell state transitions, showing it controls RNA stability to switch between regenerative and differentiated states.

Danicamtiv increases myosin recruitment and alters the chemomechanical cross bridge cycle in cardiac muscle

This study investigates how Danicamtiv increases force and alters cardiac muscle contraction kinetics by modulating myosin function and cross bridge dynamics in cardiac tissue.

Correcting dilated cardiomyopathy with fibroblast-targeted p38 deficiency

This study shows that targeting p38 in cardiac fibroblasts can reverse fibrosis and improve cardiomyocyte function in a mouse model of dilated cardiomyopathy.

dATP Elevation Induces Myocardial Metabolic Remodeling to Support Improved Cardiac Function

This study shows that elevating dATP in cardiomyocytes improves cardiac function by enhancing contractility and metabolic flexibility through mitochondrial remodeling.

Integrating comparative modeling and accelerated simulations reveals conformational and energetic basis of actomyosin force generation

This study uses comparative modeling and accelerated simulations to reveal how ATP-hydrolysis product release correlates with force generation in the actomyosin complex.

Obesity promotes Fumonisin B1 toxicity and induces hepatitis

This study shows that obesity increases susceptibility to fumonisin B1 toxicity, leading to gut dysbiosis and severe liver inflammation.

Thick Filament Activation Is Different in Fast and Slow-Twitch Skeletal Muscle

This study uses X-ray diffraction to compare thick filament activation dynamics in fast and slow-twitch rat muscles, finding distinct structural transitions that may explain their differing contraction properties.

ATGL-dependent white adipose tissue lipolysis controls hepatocyte PPARα activity

This study shows that adipose tissue lipolysis via ATGL regulates hepatocyte PPARα activity, which is essential for ketone body production, FGF21 secretion, and BAT activation during fasting and cold exposure.

Post-translational modification patterns on β-myosin heavy chain are altered in ischemic and non-ischemic human hearts

The paper identifies PTMs on β-MHC in human hearts and shows their changes in failing hearts, suggesting acetylation levels are influenced by PTM location rather than disease type.

The hepatocyte insulin receptor is required to program rhythmic gene expression and the liver clock

This study investigates the role of the hepatocyte insulin receptor in regulating circadian gene expression and liver clock function in adult mice.

From neuron to muscle to movement: a complete biomechanical model of Hydra contractile behaviors

The paper builds a biomechanical model of Hydra that links neural activity to muscle behavior and movement, reproducing key behaviors and explaining experimental observations.

Hepatocyte-specific deletion of Pparα promotes NASH in the context of obesity

This study shows that deleting Ppar in hepatocytes promotes NASH in obese mice without glucose intolerance, highlighting the role of extra-hepatocyte PPAR in metabolic responses to HFD.