Fibroblast growth factor 21 and autophagy: A complex interplay in Parkinson disease

Kakoty, Violina; Sarathlal, K C; Tang, Ruei Dun; Yang, Chih Hao; Dubey, Sunil Kumar; Taliyan, Rajeev

doi:10.1016/j.biopha.2020.110145

Cited by 22 publications

(13 citation statements)

References 89 publications

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“…FGF21 also protects against neurodegeneration in mouse models of PD (Y. Chen, Shen, Qi, et al, 2020; Fang et al, 2020). FGF21 is neuroprotective for several neurodegenerative diseases possibly by regulating the amount of autophagy (Y. Chen, Shen, Qi, et al, 2020; Kakoty et al, 2020).…”

Section: Fgf Signaling In the Brain And Sensory Organsmentioning

confidence: 99%

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New developments in the biology of fibroblast growth factors

Ornitz

Itoh

2022

WIREs Mechanisms of Disease

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The fibroblast growth factor (FGF) family is composed of 18 secreted signaling proteins consisting of canonical FGFs and endocrine FGFs that activate four receptor tyrosine kinases (FGFRs 1-4) and four intracellular proteins (intracellular FGFs or iFGFs) that primarily function to regulate the activity of voltagegated sodium channels and other molecules. The canonical FGFs, endocrine FGFs, and iFGFs have been reviewed extensively by us and others. In this review, we briefly summarize past reviews and then focus on new developments in the FGF field since our last review in 2015. Some of the highlights in the past 6 years include the use of optogenetic tools, viral vectors, and inducible transgenes to experimentally modulate FGF signaling, the clinical use of small molecule FGFR inhibitors, an expanded understanding of endocrine FGF signaling, functions for FGF signaling in stem cell pluripotency and differentiation, roles for FGF signaling in tissue homeostasis and regeneration, a continuing elaboration of mechanisms of FGF signaling in development, and an expanding appreciation of roles for FGF signaling in neuropsychiatric diseases.

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Section: Fgf Signaling In the Brain And Sensory Organsmentioning

confidence: 99%

“…FGF21 is neuroprotective for several neurodegenerative diseases possibly by regulating the amount of autophagy (Y. Chen, Shen, Qi, et al, 2020;Kakoty et al, 2020).…”

Section: Multiple Sclerosismentioning

confidence: 99%

New developments in the biology of fibroblast growth factors

Ornitz

Itoh

2022

WIREs Mechanisms of Disease

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“…Recently, increasing evidence reveals that autophagy and autophagic dysfunction are involved in many aspects of cell physiology and pathology in neurodegenerative diseases 44,45 and there is now intense interest in identifying the role of autophagy in the process of PD. 46,47 Converging evidence from genetic, pathological and experimental studies has provided indications that the autophagy is compromised in PD. 48 In the PD patients or PD animal model, the upregulation of LC3B-II/LC3-I ratio (a hallmark of autophagosomes), the accumulation of autophagosomes, 49 and the reduction of autolysosomes induced by impaired autophagosome-lysosome fusion 50 or lysosomal depletion 49 have been observed.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen sulphide attenuates neuronal apoptosis of substantia nigra by re‐establishing autophagic flux via promoting leptin signalling in a 6‐hydroxydopamine rat model of Parkinson's disease

Zou

et al. 2021

Clin Exp Pharma Physio

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Previous studies reveal that hydrogen sulphide (H 2 S) exerts neuroprotection against neurotoxin-induced Parkinson's disease (PD), but the underlying mechanism remains elusive. The present study was aimed to investigate whether H 2 S inhibits neuronal apoptosis of substantia nigra with the involvement of autophagy via promoting leptin signalling in 6-hydroxydopamine (6-OHDA)-induced PD rats. In this study, neuronal apoptosis was analysed by TUNEL staining, the activity of caspase-3 was measured by Caspase-3 fluorometric assay kit, the expressions of Bax, Bcl-2, Beclin-1, LC3II, P62 and leptin were determined by Western blot analysis, and the numbers of autophagosomes and autolysosomes were assessed by transmission electron microscopy.Results showed that NaHS, a donor of exogenous H 2 S, mitigates 6-OHDA-induced the increases in the numbers of TUNEL-positive cells, the activity of caspase-3 and the expression of Bax, and attenuates 6-OHDA-induced a decrease in the expression of Bcl-2 in substantia nigra of rats. In addition, 6-OHDA enhanced the expressions of Beclin-1, LC3-II and P62, increased the number of autophagosomes, and decreased the number of autolysosomes in the substantia nigra, which were also blocked by administration of NaHS. Furthermore, NaHS reversed 6-OHDA-induced the downregulation of leptin expression in the substantia nigra, and treatment with leptin-OBR, a blocking antibody of leptin receptor, attenuated the inhibition of NaHS on neuronal apoptosis and the improvement of NaHS on the blocked autophagic flux in substantia nigra of 6-OHDA-treated rats. Taken together, these results demonstrated that H 2 S attenuates neuronal apoptosis of substantia nigra depending on restoring impaired autophagic flux through up-regulating leptin signalling in PD.

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“…In both in vivo and in vitro AD models, FGF21 has shown anti-inflammatory and antioxidant effects, and prevented amyloid plaque formation, neurofibrillary tangle formation, and neurodegeneration [205][206][207][208]. Moreover, FGF21 treatment led to alleviated dopaminergic neuron loss, improved mitochondrial function and behavioral ability, and decreased inflammation in PD models [209][210][211][212]. Additionally, intraperitoneal injection of R1Mab1, a pharmacological agonist of FGF21 which is an IgG humanized monoclonal antibody with agonistic activity on FGFR1, improved the motility of the ALS model mice [213].…”

Section: Fgf21mentioning

confidence: 99%

Physical Exercise-Induced Myokines in Neurodegenerative Diseases

Lee

Shin

Park

et al. 2021

IJMS

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Neurodegenerative diseases (NDs), such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS), are disorders characterized by progressive degeneration of the nervous system. Currently, there is no disease-modifying treatments for most NDs. Meanwhile, numerous studies conducted on human and animal models over the past decades have showed that exercises had beneficial effects on NDs. Inter-tissue communication by myokine, a peptide produced and secreted by skeletal muscles during exercise, is thought to be an important underlying mechanism for the advantages. Here, we reviewed studies about the effects of myokines regulated by exercise on NDs and their mechanisms. Myokines could exert beneficial effects on NDs through a variety of regulatory mechanisms, including cell survival, neurogenesis, neuroinflammation, proteostasis, oxidative stress, and protein modification. Studies on exercise-induced myokines are expected to provide a novel strategy for treating NDs, for which there are no adequate treatments nowadays. To date, only a few myokines have been investigated for their effects on NDs and studies on mechanisms involved in them are in their infancy. Therefore, future studies are needed to discover more myokines and test their effects on NDs.

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Fibroblast growth factor 21 and autophagy: A complex interplay in Parkinson disease

Cited by 22 publications

References 89 publications

New developments in the biology of fibroblast growth factors

New developments in the biology of fibroblast growth factors

Hydrogen sulphide attenuates neuronal apoptosis of substantia nigra by re‐establishing autophagic flux via promoting leptin signalling in a 6‐hydroxydopamine rat model of Parkinson's disease

Physical Exercise-Induced Myokines in Neurodegenerative Diseases

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