Pro-cachectic factors link experimental and human chronic kidney disease to skeletal muscle wasting programs

Solagna, Francesca; Tezze, Caterina; Lindenmeyer, Maja T.; Lu, Shun; Wu, Guochao; Liu, Shuya; Zhao, Yu; Mitchell, Robert D.; Meyer, Charlotte; Omairi, Saleh; Kilic, Temel; Paolini, Andrea; Ritvos, Olli; Pasternack, Arja; Matsakas, Antonios; Kylies, Dominik; Wiesch, Julian Schulze zur; Turner, Jan Eric; Wanner, Nicola; Nair, Viji; Eichinger, Felix; Menon, Rajasree; Martin, Ina V.; Klinkhammer, Barbara M.; Hoxha, Elion; Cohen, Clemens D.; Tharaux, Pierre‐Louis; Boor, Peter; Ostendorf, Tammo; Kretzler, Matthias; Sandri, Marco; Kretz, Oliver; Puelles, Victor G.; Patel, Ketan; Huber, Tobias B.

doi:10.1172/jci135821

Cited by 41 publications

(48 citation statements)

References 89 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The selective packing of miRNAs into exosomes may be a novel pharmaceutical exercise mimetic for overcoming CKD-related muscle wasting or cachexia. Solagna et al reported that an increase in activin A, a member of the TGF-β protein family, in experimental CKD mice led to muscle wasting [ 98 ], while pharmaceutical blockade of activin A reduced muscle wasting. Activin A, excreted from specific kidney fibroblasts and juxtaglomerular apparatus cells, can act as a pro-cachectic factor and accumulate in the plasma, owing to reduced kidney clearance and a vicious renal/muscle signaling cycle, thereby resulting in muscle wasting.…”

Section: Therapeutic Strategies For Muscle Wastingmentioning

confidence: 99%

“…Activin A, excreted from specific kidney fibroblasts and juxtaglomerular apparatus cells, can act as a pro-cachectic factor and accumulate in the plasma, owing to reduced kidney clearance and a vicious renal/muscle signaling cycle, thereby resulting in muscle wasting. This study provided an important model of kidney-muscle crosstalk [ 98 ].…”

Section: Therapeutic Strategies For Muscle Wastingmentioning

confidence: 99%

See 1 more Smart Citation

Muscle Wasting in Chronic Kidney Disease: Mechanism and Clinical Implications—A Narrative Review

Cheng

Huang

Kao

et al. 2022

IJMS

View full text Add to dashboard Cite

Muscle wasting, known to develop in patients with chronic kidney disease (CKD), is a deleterious consequence of numerous complications associated with deteriorated renal function. Muscle wasting in CKD mainly involves dysregulated muscle protein metabolism and impaired muscle cell regeneration. In this narrative review, we discuss the cardinal role of the insulin-like growth factor 1 and myostatin signaling pathways, which have been extensively investigated using animal and human studies, as well as the emerging concepts in microRNA- and gut microbiota-mediated regulation of muscle mass and myogenesis. To ameliorate muscle loss, therapeutic strategies, including nutritional support, exercise programs, pharmacological interventions, and physical modalities, are being increasingly developed based on advances in understanding its underlying pathophysiology.

show abstract

Section: Therapeutic Strategies For Muscle Wastingmentioning

confidence: 99%

Section: Therapeutic Strategies For Muscle Wastingmentioning

confidence: 99%

Muscle Wasting in Chronic Kidney Disease: Mechanism and Clinical Implications—A Narrative Review

Cheng

Huang

Kao

et al. 2022

IJMS

View full text Add to dashboard Cite

show abstract

“…The interaction of vascular, renal and heart diseases as is currently understood for chronic disease therefore also apply in the setting of acute illness and its repair phase, though the specifics of the interaction after critical illnesses are unique to acute injury and repair programs, probably occur at a more rapid pace than occur naturally in aging, but clearly only become a concern for patients that can survive the resuscitative phases of illness (150,151). Furthermore, the persistence of CKD progression may contribute, alongside inflammatory programs, to sarcopenia and frailty in convalescence (152).…”

Section: Cardiorenal Synergy In Chronic Cardiovascular Pathogenesismentioning

confidence: 99%

Mechanisms of Post-critical Illness Cardiovascular Disease

Owen

Patel

Parekh

et al. 2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

Prolonged critical care stays commonly follow trauma, severe burn injury, sepsis, ARDS, and complications of major surgery. Although patients leave critical care following homeostatic recovery, significant additional diseases affect these patients during and beyond the convalescent phase. New cardiovascular and renal disease is commonly seen and roughly one third of all deaths in the year following discharge from critical care may come from this cluster of diseases. During prolonged critical care stays, the immunometabolic, inflammatory and neurohumoral response to severe illness in conjunction with resuscitative treatments primes the immune system and parenchymal tissues to develop a long-lived pro-inflammatory and immunosenescent state. This state is perpetuated by persistent Toll-like receptor signaling, free radical mediated isolevuglandin protein adduct formation and presentation by antigen presenting cells, abnormal circulating HDL and LDL isoforms, redox and metabolite mediated epigenetic reprogramming of the innate immune arm (trained immunity), and the development of immunosenescence through T-cell exhaustion/anergy through epigenetic modification of the T-cell genome. Under this state, tissue remodeling in the vascular, cardiac, and renal parenchymal beds occurs through the activation of pro-fibrotic cellular signaling pathways, causing vascular dysfunction and atherosclerosis, adverse cardiac remodeling and dysfunction, and proteinuria and accelerated chronic kidney disease.

show abstract

“…Sequestering activin A in the serum of CKD mice or the downregulation of its receptor prevented muscle loss, which raises the question of whether this pathway could be exploited to prevent muscle wasting in patients with advanced CKD. 78 , 79 CKD can develop secondary to systemic disease. One example is DKD, where sustained high blood glucose levels damage the kidney.…”

Section: Cell-cell and Cell-matrix Signalingmentioning

confidence: 99%

Integrating basic science with translational research: the 13th International Podocyte Conference 2021

Lausecker

Koehler

Fresquet

et al. 2022

Kidney International

Self Cite

View full text Add to dashboard Cite

Pro-cachectic factors link experimental and human chronic kidney disease to skeletal muscle wasting programs

Cited by 41 publications

References 89 publications

Muscle Wasting in Chronic Kidney Disease: Mechanism and Clinical Implications—A Narrative Review

Muscle Wasting in Chronic Kidney Disease: Mechanism and Clinical Implications—A Narrative Review

Mechanisms of Post-critical Illness Cardiovascular Disease

Integrating basic science with translational research: the 13th International Podocyte Conference 2021

Contact Info

Product

Resources

About