Landen W. Saling Data-verified
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Researcher
faculty
Research Areas
Biography and Research Information
OverviewAI-generated summary
Landen W. Saling's research focuses on the biological sex differences in the development of cancer cachexia, a complex metabolic syndrome characterized by involuntary weight loss and muscle wasting. His work investigates the molecular and physiological alterations that occur in skeletal muscle during this condition, utilizing rodent models. Saling has published studies examining fibrosis development, mitochondrial function, and protein turnover regulators in response to cancer cachexia, highlighting differential impacts between biological sexes. His research also explores the role of specific microRNAs, such as miR-16, in regulating insulin sensitivity and muscle contractile function in a sex-dependent manner. Saling collaborates with several researchers at the University of Arkansas at Fayetteville, including Tyrone A. Washington, Seongkyun Lim, Eleanor R. Schrems, and Nicholas P. Greene, with whom he has co-authored multiple publications.
Metrics
- h-index: 4
- Publications: 10
- Citations: 85
Selected Publications
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Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia (2023)
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Development of skeletal muscle fibrosis in a rodent model of cancer cachexia (2023)
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Biological Sex Differences of Fibrosis During the Development of Cancer Cachexia (2023)
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Differential Induction Of Regulators Of Protein Turnover During C26-induced Cancer Cachexia Between Biological Sexes (2022)
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Muscle miR-16 deletion results in impaired insulin sensitivity and contractile function in a sex-dependent manner (2022)
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Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice (2021)
Collaboration Network
Top Collaborators
- 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
- Development of skeletal muscle fibrosis in a rodent model of cancer cachexia
- Growth Differentiation Factor 5 Is A Paracrine Regulator In Sarcopenic Obesity
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
- Development of skeletal muscle fibrosis in a rodent model of cancer cachexia
- Growth Differentiation Factor 5 Is A Paracrine Regulator In Sarcopenic Obesity
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
- Development of skeletal muscle fibrosis in a rodent model of cancer cachexia
- Growth Differentiation Factor 5 Is A Paracrine Regulator In Sarcopenic Obesity
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
- Development of skeletal muscle fibrosis in a rodent model of cancer cachexia
- Growth Differentiation Factor 5 Is A Paracrine Regulator In Sarcopenic Obesity
Showing 5 of 9 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
- 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 7 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
- C26 Colorectal Cancer-cachexia Implications In Muscle Contractile Function And Calcium Regulation: A Biological Sex Comparison
- Differential Induction Of Regulators Of Protein Turnover During C26-induced Cancer Cachexia Between Biological Sexes
Showing 5 of 6 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
- Development of skeletal muscle fibrosis in a rodent model of cancer cachexia
- Biological Sex Differences of Fibrosis During the Development of Cancer Cachexia
- Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice
- Development of skeletal muscle fibrosis in a rodent model of cancer cachexia
- Biological Sex Differences of Fibrosis During the Development of Cancer Cachexia
- 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
- Development of skeletal muscle fibrosis in a rodent model of cancer cachexia
- Growth Differentiation Factor 5 Is A Paracrine Regulator In Sarcopenic Obesity
- Transcriptomic Analysis Of Soleus Muscle In Response To Sarcopenic Obesity
- Differential Induction Of Regulators Of Protein Turnover During C26-induced Cancer Cachexia Between Biological Sexes
- Mitochondrial Quality Control Markers During The Onset Of Colorectal Cancer-induced Cachexia: A Biological Sex Comparison
- Development of skeletal muscle fibrosis in a rodent model of cancer cachexia
- Biological Sex Differences of Fibrosis During the Development of Cancer Cachexia
- Development of skeletal muscle fibrosis in a rodent model of cancer cachexia
- Biological Sex Differences of Fibrosis During the Development of Cancer Cachexia
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