Sarcopenia, the loss of muscle mass with aging, affects nearly one-third of the older population and is one of the main factors leading to negative health outcomes in older adults. Sarcopenia can be considered as ‘primary’ (or age-related) or as ‘secondary’ when one or more other causes are evident. Sarcopenia is based on chronic inflammatory processes, insulin resistance, obesity, mitochondrial dysfunction, and oxidative stress, and malnutrition. Sarcopenia is highly correlated with frailty and risk of falls in the elder, it also represents an important risk factor for disability and mortality. Aging is best described as a multifactorial process involving complex interactions between biological/cellular and molecular mechanisms. Given this, it is unlikely that any single or readily defined set of biomarkers will provide a valid measure of biological aging.

Sarcopenia is a syndrome in which many different elements of the immune system become activated. The ongoing inflammatory process during sarcopenia is caused by cytokines and other genes related to the immune system, closely linked to a network whose elements mutually control and regulate oneself. The pathophysiology of sarcopenia is incompletely described with multiple causes, interrelationships and complex pathways proposed. However, the possible association between inflammatory parameters and sarcopenia is poorly understood. Inflammaging, which is characterized by increased levels of proinflammatory cytokines such as IL-1-β, IL-6, and TNF-α as well as CRP, and a reduced serum level of anti-inflammatory cytokines, plays a central role within the creation and maintenance of sarcopenia states. The link between sarcopenia and immunosenescence could be explained by the increased systemic inflammation, with aberrant neutrophil migration potentially contributing to inflammaging and tissue damage. It will be important for future studies in sarcopenia to focus on the correct cell types and, in targeted approaches, the correct biological pathways. Future challenges in understanding and leveraging sarcopenia immunopathogenesis include further identification of the causal pathways, cells and factors and their functional characterization, investigation of the role of immune modifications in sarcopenia pathogenesis, and translation of fundamental discoveries into clinical practice. Thus, a clear definition of sarcopenia and a better understanding of sarcopenia immunological mechanisms will enable the development of new intervention strategies.

The aim of this Special Issue is to bring together original research and review articles discussing important immunological aspects of sarcopenia. We welcome submissions considering new ideas for the diagnosis and treatment of this disease. Research can include immunological/molecular studies, cell-based analysis, human/animal studies, signal modulating small molecules, and new sarcopenia-specific markers.

Potential topics include but are not limited to the following:

• Cell pathways connecting inflammaging and sarcopenia
• Innate and adaptive immunity in immunological mechanisms of sarcopenia
• Cellular compartments and pathways involved in the immune mechanisms of sarcopenia
• The role of cytokines in sarcopenia pathogenesis
• Oxidative stress in sarcopenia
• Potential factors of inflammation, apoptosis, and sarcopenia
• Role of mitochondria in the immune system regulation of sarcopenia
• Role and function of satellite cells in the pathogenesis of sarcopenia
• Immunological biomarkers of sarcopenia
• New therapeutic options based on the immune system for treating sarcopenia