The Pathology of Intestinal Mucosal Disruption; Implications for Muscle Loss and Physical Dependency from Late Adolescence to Octogenarians.

Background And Objectives: A pathological increase in intestinal permeability causes muscle loss and physical decline by inducing systemic inflammation and oxidative stress. However, most relevant studies investigate older adults, and the appropriate data across age spans remain elusive. This study aimed to examine the associations of intestinal permeability with muscle loss and physical decline across a large span of ages.

Probiotics' supplementation alleviates disease severity and improves postural balance by repairing intestinal leak in patients suffering from osteoarthritis: a double-blinded clinical trial.

Increased intestinal leakiness and associated systemic inflammation are potential contributors to osteoarthritis (OA) and postural imbalance in the geriatric population. To date, no successful treatment to correct postural imbalance in OA is known. We aimed to explore the effects of a multistrain probiotic upon postural imbalance in OA-affected patients.

Angiotensin-converting enzyme inhibitors attenuate circulating CAF22 and physical decline in congestive heart failure: Diagnostic implications of CAF22.

Aims: Age-associated muscle loss, termed sarcopenia is the major cause of physical disability in patients with congestive heart failure (CHF). Angiotensin-converting enzyme inhibitors (ACEi) are commonly used to treat CHF patients; however, their impacts on the neuromuscular junction (NMJ) and sarcopenia in CHF patients remain poorly understood. We aim to investigate the potential impact of ACEi on NMJ and CHF-induced sarcopenia.

Nanoparticle-delivered quercetin exhibits enhanced efficacy in eliminating iron-overloaded senescent chondrocytes.

The therapeutic potential of senolytic drugs in osteoarthritis (OA) is poorly known. Quercetin, a senolytic agent exhibits promising potential to treat OA, having limited bioavailability. We investigated the effects of Quercetin-loaded nanoparticles (Q-NP) with enhanced bioavailability in human chondrocytes mimicking OA phenotype.

Nicotinamide riboside kinase 2: A unique target for skeletal muscle and cardiometabolic diseases.

Myopathy leads to skeletal and cardiac muscle degeneration which is a major cause of physical disability and heart failure. Despite the therapeutic advancement the prevalence of particularly cardiac diseases is rising at an alarming rate and novel therapeutic targets are required. Nicotinamide riboside kinase-2 (NRK-2 or NMRK2) is a muscle-specific β1-integrin binding protein abundantly expressed in the skeletal muscle while only a trace amount is detected in the healthy cardiac muscle.