Mitochondrial Biogenesis in Skeletal Muscle.

Mitochondrial biogenesis refers to the synthesis of nuclear- and mitochondrially encoded proteins, along with phospholipids, that aid in the expansion of the mitochondrial network. In skeletal muscle, mitochondria are organized as a reticulum, as this ideal morphology complements the elongated shape of a myofibre. This allows for efficient substrate diffusion and supports the vigorously dynamic metabolic capabilities of this tissue type.

Role of Prohibitins as Guardians of mitochondrial homeostasis.

Mitochondria are complex organelles critical to the maintenance of cellular homeostasis. Central to this regulation are Prohibitins (PHBs), a novel set of proteins involved in several mitochondrial quality control pathways, including protein folding, biogenesis, and mitophagy. PHBs mediate various cellular responses including cell survival and myogenesis, suggesting that their roles are intricate and multifaceted.

Effect of aging, endurance training, and denervation on innate immune signaling in skeletal muscle.

Skeletal muscle function relies on mitochondria for energy and for mediating its unique adaptive plasticity. The NLRP3 inflammasome complex is an innate immune mechanism that responds to mitochondrial damage-associated molecular patterns (DAMPs); however, its activity relative to mitochondrial dysfunction in muscle requires exploration. The purpose of this study was to characterize immune signaling and mitochondrial function in muscle during aging, endurance training, and disuse induced by denervation.

Adaptations in mitochondrial quality control and interactions with innate immune signaling within skeletal muscle: A narrative review.

Skeletal muscle health and function are essential determinants of metabolic health, physical performance, and overall quality of life. The quality of skeletal muscle is heavily dependent on the complex mitochondrial reticulum that contributes toward its unique adaptability. It is now recognized that mitochondrial perturbations can activate various innate immune pathways, such as the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome complex by propagating inflammatory signaling in response to damage-associated molecular patterns (DAMPs).

Padua Days on Muscle and Mobility Medicine, March 25-29, 2025, Hotel Petrarca, Euganean Thermae, Italy: Program and Abstracts.

Medium-sized scientific conferences held in hotels large enough to accommodate all participants increase opportunities for constructive discussion during breaks, and for evenings that bring together young and senior experts of basic sciences and clinical specialties. Time for group discussions offer opportunities for new collaborations and for jobs for young researchers. Since 1991 the Padova Muscle Days have offered collaborative opportunities that have matured into innovative multidisciplinary results to the point that it came naturally for us to underline it with a neologism now included in the title of the 2025 event: "Mobility Medicine".

Deducing Reaction and Diffusion Depths of Near-Interfacial Solvated Electrons from pH-Dependent Product Evaporation.

Near-interfacial electrons in water can be produced by bombarding an aqueous microjet in vacuum with gas-phase sodium atoms. These Na atoms immediately ionize into Na and e, which can then react with surface-active molecules that preferentially populate the surface. We carried out these experiments by reacting e with the surfactant benzyltrimethylammonium (BTMA) in a 6.

Focus on the Forgotten Organelle: Regulation of Lysosomes in Skeletal Muscle.

Research on the role of the lysosome as the terminal organelle in autophagy and in communicating with other organelles in skeletal muscle is in its infancy. We hypothesize that the lysosome can adapt positively to exercise to improve the clearance of cargo, like dysfunctional mitochondria, within muscle, representing an important therapy for protein homeostasis in aging and muscle disuse.

Sulforaphane treatment mimics contractile activity-induced mitochondrial adaptations in muscle myotubes.

Mitochondria are metabolic hubs that govern skeletal muscle health. Although exercise has been established as a powerful inducer of quality control processes that ultimately enhance mitochondrial function, there are currently limited pharmaceutical interventions available that emulate exercise-induced mitochondrial adaptations. To investigate a novel candidate for this role, we examined sulforaphane (SFN), a naturally occurring compound found in cruciferous vegetables.

Sulforaphane, Urolithin A, and ZLN005 induce time-dependent alterations in antioxidant capacity, mitophagy, and mitochondrial biogenesis in muscle cells.

Efficient signal transduction that mediates mitochondrial turnover is a strong determinant of metabolic health in skeletal muscle. Of these pathways, our focus was aimed towards the enhancement of antioxidant capacity, mitophagy, and mitochondrial biogenesis. While physical activity is an excellent inducer of mitochondrial turnover, its ability to ubiquitously activate and enhance mitochondrial turnover prevents definitive differentiation of the contribution made by each pathway.

Treatment persistence, adherence and healthcare resource utilisation for iGlarLixi versus basal-bolus insulin or premixed insulin in older adult ethnic minorities with type 2 diabetes: SoliEthnicity study.

Aims: Most type 2 diabetes (T2D) studies have predominantly enrolled White people aged <65 years. This retrospective study evaluated outcomes for iGlarLixi (fixed-ratio combination [FRC] of insulin glargine 100 U/mL and lixisenatide) versus basal-bolus or premixed insulin in African American, Asian and Hispanic adults with T2D aged ≥65 years.

Methods: Medicare claims data were assessed from beneficiaries receiving basal insulin who newly initiated iGlarLixi, basal-bolus insulin, or premixed insulin between 7/1/2019 and 12/30/2021.

Probing the interfacial structure of aqueous surfactants through helium atom evaporation.

Dissolved helium atoms evaporate from liquids in super-Maxwellian speed distributions because their interactions are too weak to enforce full thermal equilibration at the surface as they are "squeezed" out of solution. The excess speeds of these He atoms reflect their final interactions with solvent and solute molecules at the surfaces of water and other liquids. We extend this observation by monitoring He atom evaporation from salty water solutions coated with surfactants.

Dimorphic effect of TFE3 in determining mitochondrial and lysosomal content in muscle following denervation.

Background: Muscle atrophy is a common consequence of the loss of innervation and is accompanied by mitochondrial dysfunction. Mitophagy is the adaptive process through which damaged mitochondria are removed via the lysosomes, which are regulated in part by the transcription factor TFE3. The role of lysosomes and TFE3 are poorly understood in muscle atrophy, and the effect of biological sex is widely underreported.

The effects of daily dose of intense exercise on cardiac responses and atrial fibrillation.

Atrial fibrillation (AF) is a supraventricular tachyarrhythmia that is strongly associated with cardiovascular (CV) disease and sedentary lifestyles. Despite the benefits of exercise on overall health, AF incidence in high-level endurance athletes rivals that of CV disease patients, suggesting a J-shaped relationship with AF. To investigate the dependence of AF vulnerability on exercise, we varied daily swim durations (120, 180 or 240 min day ) in 7-week-old male CD1 mice.

Journey to anticoagulant access following payer rejection of apixaban.

Objectives: To investigate the journey to oral anticoagulant (OAC) access following formulary-related rejection of apixaban (Eliquis) and evaluate characteristics associated with failure to achieve OAC access among patients with atrial fibrillation (AF).

Study Design: Retrospective study using the Optum Market Clarity Data from January 2016 through February 2020.

Methods: Patients had at least 1 claim rejection for apixaban due to prior authorization (PA), formulary exclusion (FE), or quantity limit (QL) and at least 1 AF diagnosis on or before the rejected claim.

Muscle mitochondrial transplantation can rescue and maintain cellular homeostasis.

Mitochondria control cellular functions through their metabolic role. Recent research that has gained considerable attention is their ability to transfer between cells. This has the potential of improving cellular functions in pathological or energy-deficit conditions, but little is known about the role of mitochondrial transfer in sustaining cellular homeostasis.

Exercise, mitochondrial dysfunction and inflammasomes in skeletal muscle.

In the broad field of inflammation, skeletal muscle is a tissue that is understudied. Yet it represents about 40% of body mass in non-obese individuals and is therefore of fundamental importance for whole body metabolism and health. This article provides an overview of the unique features of skeletal muscle tissue, as well as its adaptability to exercise.

A Real-World Evaluation of Primary Medication Nonadherence in Patients with Nonvalvular Atrial Fibrillation Prescribed Oral Anticoagulants in the United States.

Background: Nonadherence to oral anticoagulants (OACs) is a challenge to stroke risk reduction in patients with nonvalvular atrial fibrillation (NVAF). Data on primary medication nonadherence (PMN) in NVAF are lacking.

Objectives: Our aim was to assess the rates and predictors of PMN among NVAF patients who were newly prescribed an OAC.

Activating transcription factor 4 regulates mitochondrial content, morphology, and function in differentiating skeletal muscle myotubes.

Mitochondrial function is widely recognized as a major determinant of health, emphasizing the importance of understanding the mechanisms promoting mitochondrial quality in various tissues. Recently, the mitochondrial unfolded protein response (UPR) has come into focus as a modulator of mitochondrial homeostasis, particularly in stress conditions. In muscle, the necessity for activating transcription factor 4 (ATF4) and its role in regulating mitochondrial quality control (MQC) have yet to be determined.

Creation and Reaction of Solvated Electrons at and near the Surface of Water.

Solvated electrons (e) are among nature's most powerful reactants, with over 2600 reactions investigated in bulk water. These electrons can also be created at and near the surface of water by exposing an aqueous microjet in vacuum to gas-phase sodium atoms, which ionize into e and Na within the top few layers. When a reactive surfactant is added to the jet, the surfactant and e become coreactants localized in the interfacial region.

Relationship between Mitochondrial Quality Control Markers, Lower Extremity Tissue Composition, and Physical Performance in Physically Inactive Older Adults.

Altered mitochondrial quality and function in muscle may be involved in age-related physical function decline. The role played by the autophagy-lysosome system, a major component of mitochondrial quality control (MQC), is incompletely understood. This study was undertaken to obtain initial indications on the relationship between autophagy, mitophagy, and lysosomal markers in muscle and measures of physical performance and lower extremity tissue composition in young and older adults.

Scientific meeting report: International Biochemistry of Exercise 2022.

Exercise is one of the only nonpharmacological remedies known to counteract genetic and chronic diseases by enhancing health and improving life span. Although the many benefits of regular physical activity have been recognized for some time, the intricate and complex signaling systems triggered at the onset of exercise have only recently begun to be uncovered. Exercising muscles initiate a coordinated, multisystemic, metabolic rewiring, which is communicated to distant organs by various molecular mediators.

Denervation induces mitochondrial decline and exacerbates lysosome dysfunction in middle-aged mice.

With age, skeletal muscle undergoes a progressive decline in size and quality. Imbalanced mitochondrial turnover and the resultant dysfunction contribute to these phenotypic alterations. Motor neuron denervation (Den) is a contributor to the etiology of muscle atrophy associated with age.