Can Muscle-Kidney Crosstalk Slow Progression of CKD?

Rondon‐Berrios, Helbert; Wang, Yanlin

doi:10.1681/asn.2014060566

Cited by 14 publications

(7 citation statements)

References 17 publications

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“…A similar phenomenon on the slowing of renal functional decline has been observed in a mouse model from products of the skeletal muscle [11]. Perhaps the effect of the functioning AVF is mediated indirectly through what happens to skeletal muscle post fistula creation, as there is a very metabolically active muscle 'secretome' as recently discussed by Rondon-Berrios et al [12]. Thus, there is biological plausibility of stabilization of renal function or a slowing of its loss after the creation of a functional AV fistula.…”

Section: F I G U R Esupporting

confidence: 62%

Arteriovenous fistula creation may slow estimated glomerular filtration rate trajectory

Golper¹,

Hartle²,

Bian³

2015

Nephrol. Dial. Transplant.

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Section: F I G U R Esupporting

confidence: 62%

Arteriovenous fistula creation may slow estimated glomerular filtration rate trajectory

Golper¹,

Hartle²,

Bian³

2015

Nephrol. Dial. Transplant.

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“…Accumulating evidence suggests that skeletal muscle is also involved in the crosstalk between other organs (69,70). …”

Section: Muscle and Organ Cross Talk Through Microvesiclesmentioning

confidence: 99%

“…Organ crosstalk may also be achieved by the release of miRNAs packaged in exosomes that are transported through circulation and delivery to other tissues ( 67 , 68 ). Accumulating evidence suggests that skeletal muscle is also involved in the crosstalk between other organs ( 69 , 70 ).…”

Section: Muscle and Organ Cross Talk Through Microvesiclesmentioning

confidence: 99%

Extracellular vesicle microRNAs mediate skeletal muscle myogenesis and disease

Wang

2016

Biomedical Reports

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Skeletal muscle function is important for good health and independent living, and has been subject to numerous studies focused on skeletal muscle development, function and metabolism. However, progressive and degenerative changes in skeletal muscle function often occur following physiological and pathological stress, and these lead to the progression of diabetes, obesity, chronic kidney disease, and cardiovascular or respiratory diseases. Identifying the mechanisms that influence the processes regulating skeletal muscle function is a key priority. Recently, studies have demonstrated that microRNAs (miRNAs) play important roles in regulating biological processes. For instance, exosomes are key tools for communication between cells. Therefore, by determining how select miRNAs are transported to target organs and initiate their effects, these results will help explain muscle and organ crosstalk, improve our understanding and application of current therapeutic approaches and lead to the identification of new therapeutic strategies and targets aimed at maintaining and/or improving skeletal muscle health.

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“…2,3 Recent studies suggest that attenuating skeletal muscle atrophy improves kidney recovery after injury by reducing renal fibrosis. 4,5 The mechanism underlying the benefits of these muscle-derived microRNAs remains unknown, and the adeno-associated virus (AAV)mediated microRNA transfer from skeletal muscles to other organs is poorly understood.…”

mentioning

confidence: 99%

Exogenous miR-29a Attenuates Muscle Atrophy and Kidney Fibrosis in Unilateral Ureteral Obstruction Mice

Wang

et al. 2020

Human Gene Therapy

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Renal fibrosis leads to end-stage renal disease, but antifibrotic drugs are difficult to develop. Chronic kidney disease often results in muscle wasting, and thereby increases morbidity and mortality. In this work, adeno-associated virus (AAV)mediated overexpressing miR-29a was hypothesized to counteract renal fibrosis and muscle wasting through muscle-kidney crosstalk in unilateral ureteral obstruction (UUO) mice. miR-29a level was downregulated in the kidney and skeletal muscle of UUO mice. The secretion of exosome-encapsulated miR-29a increased in cultured skeletal muscle satellite cells and HEK293 renal cells after stimulation with serum from UUO mice. This result was confirmed by qPCR and microRNA deep sequencing in the serum exosomes of mice with obstructed ureters. A recombinant AAV-miR-29a was generated to overexpress miR-29a and injected into the tibialis anterior muscle of the mice 2 weeks before UUO surgery. AAV-miR-29a abrogated the UUO-induced upregulation of YY1 and myostatin in skeletal muscles. Renal fibrosis was also partially improved in the UUO mice with intramuscular AAV-miR-29a transduction. AAV-miR-29a overexpression reversed the increase in transforming growth factor b, fibronectin, alpha-smooth muscle actin, and collagen 1A1 and 4A1 levels in the kidney of UUO mice. AAV-green fluorescent protein was applied to trace the AAV route in vivo, and fluorescence was significantly visible in the injected/uninjected muscles and in the kidneys. In conclusion, intramuscular AAV-miR-29a injection attenuates muscle wasting and ameliorates renal fibrosis by downregulating several fibrotic-related proteins in UUO mice.

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Can Muscle-Kidney Crosstalk Slow Progression of CKD?

Cited by 14 publications

References 17 publications

Arteriovenous fistula creation may slow estimated glomerular filtration rate trajectory

Arteriovenous fistula creation may slow estimated glomerular filtration rate trajectory

Extracellular vesicle microRNAs mediate skeletal muscle myogenesis and disease

Exogenous miR-29a Attenuates Muscle Atrophy and Kidney Fibrosis in Unilateral Ureteral Obstruction Mice

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