Match tier
Likely match
Presence
Current · Arkansas
Last published
2025
Sources
OpenAlex · ORCID
Refreshed
2026-08-15
F
Francielly Morena da Silva
This is a likely match — the affiliation was inferred from OpenAlex, ORCID, and web sources but has not been fully confirmed. Treat with appropriate caution.
Post-Doctoral Fellow
Postdoc Researcher
12 h-index
38 pubs
438 cited
Research Areas
Biomedical Subjects
Links
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 has explored transcriptional changes in skeletal muscle in response to various stimuli, including acute growth signals, exercise, and aging. She has published studies examining sex-based differences in muscle response to disuse atrophy and cancer cachexia, noting that female mice may exhibit exacerbated catabolic signaling and preserved muscle quality in certain contexts. Further research has delved into the interplay between circadian rhythms and inflammation-induced skeletal muscle atrophy. Da Silva's scholarship also includes an analysis of the molecular landscape following exercise in humans, identifying MYC as a factor sufficient for muscle growth. Her scholarship metrics include an h-index of 11, with 38 total publications and 413 citations. She has collaborated extensively with researchers at the University of Arkansas at Fayetteville, including Tyrone A. Washington, Nicholas P. Greene, Ana Regina Cabrera, and Eleanor R. Schrems.
Metrics
- h-index: 12
- Publications: 38
- Citations: 438
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
Nicholas P. Greene
University of Arkansas at Fayetteville
32 shared publications
In database
- 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
- Inflammation o'clock: interactions of circadian rhythms with inflammation‐induced skeletal muscle atrophy
Showing 5 of 32 shared publications
Ana Regina Cabrera
University of Arkansas at Fayetteville
26 shared publications
In database
- 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 26 shared publications
Tyrone A. Washington
University of Arkansas at Fayetteville
24 shared publications
In database
- 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
Kevin A. Murach
University of Arkansas at Fayetteville
24 shared publications
In database
- 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
- 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
Eleanor R. Schrems
University of Arkansas at Fayetteville
22 shared publications
In database
- 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
Megan E. Rosa‐Caldwell
University of Arkansas at Fayetteville
15 shared publications
In database
- 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
Seongkyun Lim
University of Arkansas at Fayetteville
15 shared publications
In database
- 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
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia
Showing 5 of 15 shared publications
Stavroula Tsitkanou
University of Arkansas at Fayetteville
12 shared publications
In database
- 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
- 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 12 shared publications
Ronald G. Jones
University of Arkansas at Fayetteville
11 shared publications
In database
- 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
Sabin Khadgi
University of Arkansas at Fayetteville
8 shared publications
In database
- 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
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
Showing 5 of 8 shared publications
J. William Deaver
University of Arkansas at Fayetteville (US)
6 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
Yuan Wen
University of Kentucky (US)
6 shared publications
- 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
- Skeletal muscle methylome-transcriptome disruptions during the onset and progression of colorectal cancer-induced cachexia
Showing 5 of 6 shared publications
Pieter J. Koopmans
University of Arkansas at Fayetteville
6 shared publications
In database
- 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
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Showing 5 of 6 shared publications
Calvin Peterson
University of Arkansas at Fayetteville
5 shared publications
In database
- 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
- 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
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Ruqaiza Muhyudin
University of Arkansas at Fayetteville
5 shared publications
In database
- 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
- 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
- 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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