Transforming Growth Factor-Beta in Skeletal Muscle Wasting

Abstract

Transforming growth factor-beta (TGF-β) is part of a family of molecules that is present in many body tissues and performs many different functions. Evidence has been obtained from mice and human cancer patients with bony metastases and non-metastatic disease, as well as pediatric burn patients, that inflammation leads to bone resorption and release of TGF-β from the bone matrix with paracrine effects on muscle protein balance, possibly mediated by the generation of reactive oxygen species. Whether immobilization, which confounds the etiology of bone resorption in burn injury, also leads to the release of TGF-β from bone contributing to muscle wasting in other conditions is unclear. The use of anti-resorptive therapy in both metastatic cancer patients and pediatric burn patients has been successful in the prevention of muscle wasting, thereby creating an additional therapeutic niche for this class of drugs. The liberation of TGF-β may be one way in which bone helps to control muscle mass, but further investigation will be necessary to assess whether the rate of bone resorption is the determining factor for the release of TGF-β. Moreover, whether different resorptive conditions, such as immobilization and hyperparathyroidism, also involve TGF-β release in the pathogenesis of muscle wasting needs to be investigated.

Indoxyl sulfate induced frailty in patients with end-stage renal disease by disrupting the PGC-1α–FNDC5 axis

“…The transcriptional level of TGF-β3 and TGF-β receptors increased in 5/6 nephrectomized mice. TGF-β has been regarded as the profibrotic hormone, and its release from the extracellular matrix could be induced by a specific stimulating factor such as oxidative stress or insulin resistance commonly noticed in the uremic milieu [18][19][20][21]. The activity of PPARγ could downregulate TGF-β via direct inhibition or the release of microRNA (miRNA) associated with fibrosis, such as miR-133-5p [22,23].…”

Exploring the emerging bidirectional association between inflamm‐aging and cellular senescence in organismal aging and disease

“…Similarly, transforming growth factor‐beta (TGF‐β) is another important member of the anti‐inflammatory network that is observed to increase in octogenarians and centenarians 61,62 . TGF‐β signaling also appears to be regulatory in age‐related diseases such as stroke, sarcopenia, and osteoarthritis 63–65 . Although an increase in anti‐inflammatory cytokines with age might appear counterintuitive to inflamm‐aging, it must be noted that such changes in pro‐ and anti‐inflammatory cytokine networks are not unidirectional but dynamic that coexist as part of a feedback loop.…”

“…61,62 TGF-β signaling also appears to be regulatory in age-related diseases such as stroke, sarcopenia, and osteoarthritis. [63][64][65] Although an increase in anti-inflammatory cytokines with age might appear counterintuitive to inflamm-aging, it must be noted that such changes in pro-and anti-inflammatory cytokine networks are not unidirectional but dynamic that coexist as part of a feedback loop.…”

Biologiczne wspomaganie leczenia ortopedycznego

“…[48] Tabela 5. Czynniki wzrostu wydzielane przez płytki krwi i pełnione przez nie funkcje we wspomaganiu leczenia ortopedycznego [49][50][51]. włóknisto-naczyniowej w ostrym gojeniu ścięgien i kości [8], zwiększeniu gęstości mineralnej kości [9], poprawianiu funkcjonowania mięśni i zmniejszaniu nacieków tłuszczowych w mięśniach oraz zwiększeniu powierzchni chrząstki włóknistej [10].…”