Francielly Morena da Silva Data-verified
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Post-Doctoral Fellow
postdoc
Research Areas
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Biography and Research Information
OverviewAI-generated summary
Francielly Morena da Silva's research investigates molecular mechanisms underlying skeletal muscle adaptation and atrophy, with a particular focus on cancer cachexia and disuse atrophy. Her work utilizes multi-transcriptome analysis to identify global and regulatory networks involved in muscle growth and adaptation, including the role of MYC. Silva has explored sex-based differences in skeletal muscle responses, finding that female mice may exhibit exacerbated catabolic signaling during disuse atrophy and distinct transcriptional disruptions compared to males during cancer cachexia progression. Her research also examines the impact of aging on exercise adaptation and the interplay between circadian rhythms and inflammation in skeletal muscle atrophy. She has published 38 papers, accumulating 368 citations, and holds an h-index of 10. Silva collaborates extensively with researchers at the University of Arkansas at Fayetteville, including Tyrone A. Washington, Ana Regina Cabrera, Eleanor R. Schrems, and Nicholas P. Greene.
Metrics
- h-index: 11
- Publications: 38
- Citations: 389
Selected Publications
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Skeletal muscle methylome-transcriptome disruptions during the onset and progression of colorectal cancer-induced cachexia (2025)
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The Age-Dependent Resident Myonuclear Multi-Omic Response to a Skeletal Muscle Hypertrophic Stimulus (2025)
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Transcriptomic analysis demonstrates moderators of muscle quality are altered in age-related sarcopenic obesity (2025)
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Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females (2025)
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Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice (2025)
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Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice (2025)
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The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth (2024)
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Transcriptional analysis of cancer cachexia: conserved and unique features across preclinical models and biological sex (2024)
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Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice (2024)
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Exploring heterogeneity: a dive into preclinical models of cancer cachexia (2024)
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The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth (2024)
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Supplemental table 6 (2023)
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Supplemental table 1 (2023)
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Supplemental table 3 (2023)
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Supplemental table 2 (2023)
Collaboration Network
Top Collaborators
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- Female mice may have exacerbated catabolic signalling response compared to male mice during development and progression of disuse atrophy
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice
- The time-course of cancer cachexia onset reveals biphasic transcriptional disruptions in female skeletal muscle distinct from males
Showing 5 of 38 shared publications
- Female mice may have exacerbated catabolic signalling response compared to male mice during development and progression of disuse atrophy
- Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice
- The time-course of cancer cachexia onset reveals biphasic transcriptional disruptions in female skeletal muscle distinct from males
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia
- Muscle miR-16 deletion results in impaired insulin sensitivity and contractile function in a sex-dependent manner
Showing 5 of 28 shared publications
- Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice
- The time-course of cancer cachexia onset reveals biphasic transcriptional disruptions in female skeletal muscle distinct from males
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia
- Muscle miR-16 deletion results in impaired insulin sensitivity and contractile function in a sex-dependent manner
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
Showing 5 of 27 shared publications
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- The time-course of cancer cachexia onset reveals biphasic transcriptional disruptions in female skeletal muscle distinct from males
- Inflammation o'clock: interactions of circadian rhythms with inflammation‐induced skeletal muscle atrophy
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
Showing 5 of 27 shared publications
- Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice
- The time-course of cancer cachexia onset reveals biphasic transcriptional disruptions in female skeletal muscle distinct from males
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia
- Muscle miR-16 deletion results in impaired insulin sensitivity and contractile function in a sex-dependent manner
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
Showing 5 of 24 shared publications
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- Female mice may have exacerbated catabolic signalling response compared to male mice during development and progression of disuse atrophy
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice
- The time-course of cancer cachexia onset reveals biphasic transcriptional disruptions in female skeletal muscle distinct from males
Showing 5 of 20 shared publications
- Female mice may have exacerbated catabolic signalling response compared to male mice during development and progression of disuse atrophy
- Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice
- The time-course of cancer cachexia onset reveals biphasic transcriptional disruptions in female skeletal muscle distinct from males
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia
- Muscle miR-16 deletion results in impaired insulin sensitivity and contractile function in a sex-dependent manner
Showing 5 of 15 shared publications
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- Biological sex divergence in transcriptomic profiles during the onset of hindlimb unloading-induced atrophy
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
Showing 5 of 13 shared publications
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- The time-course of cancer cachexia onset reveals biphasic transcriptional disruptions in female skeletal muscle distinct from males
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Transcriptional analysis of cancer cachexia: conserved and unique features across preclinical models and biological sex
Showing 5 of 11 shared publications
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
Showing 5 of 10 shared publications
- Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia
- Muscle miR-16 deletion results in impaired insulin sensitivity and contractile function in a sex-dependent manner
- Growth Differentiation Factor 5 Is A Paracrine Regulator In Sarcopenic Obesity
- C26 Colorectal Cancer-cachexia Implications In Muscle Contractile Function And Calcium Regulation: A Biological Sex Comparison
Showing 5 of 8 shared publications
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- At the Nexus Between Epigenetics and Senescence: The Effects of Senolytic ( <scp>BI01</scp> ) Administration on <scp>DNA</scp> Methylation Clock Age and the Methylome in Aged and Regenerated Skeletal Muscle
Showing 5 of 8 shared publications
- Female mice may have exacerbated catabolic signalling response compared to male mice during development and progression of disuse atrophy
- Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia
- Muscle miR-16 deletion results in impaired insulin sensitivity and contractile function in a sex-dependent manner
- C26 Colorectal Cancer-cachexia Implications In Muscle Contractile Function And Calcium Regulation: A Biological Sex Comparison
Showing 5 of 7 shared publications
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- MicroRNA control of the myogenic cell transcriptome and proteome: the role of miR-16
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- At the Nexus Between Epigenetics and Senescence: The Effects of Senolytic ( <scp>BI01</scp> ) Administration on <scp>DNA</scp> Methylation Clock Age and the Methylome in Aged and Regenerated Skeletal Muscle
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
Showing 5 of 7 shared publications
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
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