Antibodies against tumor necrosis factor (TNF) and IL-6 receptor are the most effective available therapies against rheumatoid arthritis (RA). However, no cure for RA exists. In work published in Science Translational Medicine, scientists from Sanofi R&D (Sanofi SA) investigated whether dual inhibition of TNF and IL-6 could improve the therapeutic efficacy against RA.

Bone-resorbing osteoclasts are key players in bone remodeling and their dysfunction has been implicated in several bone disorders such as fibrous dysplasia. Osteoclasts derive from monocytes stimulated by several cytokines, such as M-CSF and RANKL.

The lack of dystrophin causes Duchenne muscular dystrophy (DMD), a muscle-wasting disease that is often accompanied by heart failure due to cardiomyocyte death and fibrosis that can lead to death of the patient. It has been proven that telomere shortening is a hallmark of DMD cardiomyocytes. Researchers from the Stanford School of Medicine have recently investigated whether preventing telomere shortening and attrition may be a therapeutic approach in DMD.

Osteoarthritis (OA) is the most common joint disease and a leading cause of disability worldwide. Its treatment is still elusive due to difficulties with early diagnoses and patient risk identification. This leads to a need for reliable biomarkers for OA prognosis or to identify patients at risk of progression.

An Icelandic genome-wide association study that linked variants in a gene which regulates retinoic acid synthesis to severe osteoarthritis (OA) of the hands, has led on to the discovery of an anti-inflammatory role for the vitamin A metabolite and pointed to a new class of potentially disease-modifying drugs. A proof-of-concept clinical trial of talarozole, a retinoic acid metabolism blocking agent, is now taking place to assess if increasing retinoic acid production suppresses inflammation in the joint tissues of patients with OA.

The first in vivo cell atlas of senescent tissue in skeletal muscle has identified the damaging properties of these cells and explained why they block muscle regeneration. According to a study at Pompeu Fabra University led by scientists from Altos Labs Inc., cell damage caused the senescence of the cells, which secreted toxic substances into the surrounding microenvironment, causing fibrosis and preventing tissue regeneration.

To date, there are no current orally available compounds that promote bone formation for treating osteoporosis; most treatments act by inhibiting osteoclastic bone resorption, leading to increased bone mineral density and reduced hip fracture rate in a modest way. Analogues of parathyroid hormone (PTH) are the most frequently used bone anabolic agents, which even though effective, they require daily injections.