Francielly Morena da Silva
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Post-Doctoral Fellow
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Francielly Morena da Silva's research investigates molecular mechanisms underlying skeletal muscle atrophy, particularly in the context of aging, disuse, and cancer cachexia. Her work utilizes multi-transcriptome analysis to identify regulatory networks and molecular signatures associated with these conditions. Recent studies have explored sex-based differences in catabolic signaling and transcriptional disruptions during muscle atrophy progression, with findings suggesting females may exhibit distinct responses compared to males. Silva's publications also examine the interplay between circadian rhythms and inflammation-induced muscle atrophy, as well as molecular adaptations to exercise with aging. Her scholarship metrics include an h-index of 12, 38 total publications, and 462 total citations. She collaborates extensively with researchers at the University of Arkansas at Fayetteville, including Tyrone A. Washington, Nicholas P. Greene, Ana Regina Cabrera, and Eleanor R. Schrems, with whom she shares a significant number of publications.
Metrics
- h-index: 12
- Publications: 38
- Citations: 465
Positions
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Post-Doctoral Fellow 2024–presentUniversity of Florida Physiology and Aging ORCID
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Post-Doctoral Fellow publications 2021–2025University of Arkansas at Fayetteville ORCID
Selected Publications
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Differential impact of cancer- and chemotherapy-induced cachexia: a comparative analysis in a preclinical model of colorectal cancer by biological sex (2026)
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Exercise training prior to and during cancer in mice preserves muscle mass, reduces tumour weight and suppresses molecular mediators of cachexia (2026)
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The Age‐Dependent Resident Myonuclear Multi‐Omic Response to an Acute Skeletal Muscle Hypertrophic Stimulus in Mice (2026)
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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)
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 33 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 26 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 24 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 22 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 16 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
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing 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
- Transcriptional analysis of cancer cachexia: conserved and unique features across preclinical models and biological sex
- 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 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 9 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
- The Age-Dependent Resident Myonuclear Multi-Omic Response to a Skeletal Muscle Hypertrophic Stimulus
Showing 5 of 7 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
- Males, But Not Females, Demonstrate Mitochondrial Dysfunction In The C26 Model Of Cancer Cachexia
Showing 5 of 6 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
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
Showing 5 of 6 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
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
Showing 5 of 6 shared publications
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- Transcriptional analysis of cancer cachexia: conserved and unique features across preclinical models and biological sex
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
Showing 5 of 6 shared publications
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