GO:0034103 regulation of tissue remodeling: Biological Process, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0034103 regulation of tissue remodeling is defined as any process that modulates the frequency, rate, or extent of tissue remodeling.
• Tissue remodeling is a dynamic process that reshapes organs in response to physiological cues such as circadian rhythms, nutrient availability, and inflammation [1,2,7].
• Key regulatory mechanisms include circadian control of bone remodeling, beiging of perivascular adipose tissue, and epigenetic regulation of adipose thermogenesis [1,2,6].
• Dysregulation of tissue remodeling contributes to metabolic bone disease, vascular pathology, and cancer progression [3,7,8].
• CRISPR-based models (knockout, point mutation, knock-in, overexpression) enable causal interrogation of genes regulating tissue remodeling [4,5].
• Understanding GO:0034103 has therapeutic implications for osteoporosis, obesity, cardiovascular disease, and tissue regeneration [7,8].
Description
Tissue remodeling is a fundamental biological process that governs the dynamic reorganization of organs and tissues throughout life. The Gene Ontology term GO:0034103, regulation of tissue remodeling, encompasses any process that modulates the frequency, rate, or extent of tissue remodeling. This regulatory control is essential for maintaining tissue homeostasis, adapting to environmental challenges, and repairing damage. Dysregulation of tissue remodeling underlies a wide range of pathological conditions, including osteoporosis, vascular disease, and metabolic disorders [3,7,8]. Understanding the molecular players and signaling pathways that regulate tissue remodeling is therefore critical for developing targeted therapeutic interventions. Recent studies have highlighted the importance of circadian rhythms, nutrient sensing, and epigenetic mechanisms in controlling tissue remodeling processes [1,6,7]. For example, circadian regulation of bone remodeling ensures that bone formation and resorption occur at optimal times, while beiging of perivascular adipose tissue influences vascular remodeling and inflammation [1,2]. These findings underscore the complexity and physiological relevance of GO:0034103. In this article, we provide a comprehensive overview of the regulation of tissue remodeling, covering its definition, key genes, disease associations, and research methodologies, with a focus on CRISPR-based approaches for functional interrogation.
regulation of tissue remodeling At A Glance
| GO ID | GO:0034103 |
|---|---|
| GO term | regulation of tissue remodeling |
| Ontology | biological_process |
| Synonym | regulation of tissue remodelling |
| Definition | Any process that modulates the frequency, rate, or extent of tissue remodeling. |
| Major function | Modulation of tissue reorganization in response to physiological and pathological cues. |
| Related processes | Bone remodeling, adipose tissue remodeling, vascular remodeling, endometrial remodeling. |
| Regulatory inputs | Circadian rhythms, nutrients, hormones, inflammatory cytokines, epigenetic modifiers. |
| Disease relevance | Osteoporosis, obesity, cardiovascular disease, cancer, metabolic disorders. |
What Is GO:0034103?
According to the Gene Ontology, GO:0034103 regulation of tissue remodeling is defined as any process that modulates the frequency, rate, or extent of tissue remodeling. This term is a biological process and includes both positive and negative regulation of the remodeling process. Tissue remodeling itself refers to the reorganization or restructuring of existing tissue, which can involve changes in cell composition, extracellular matrix, and tissue architecture. The regulation of this process ensures that remodeling occurs appropriately in response to developmental, physiological, or pathological stimuli.
Why Is regulation of tissue remodeling Important in Cell Biology?
The regulation of tissue remodeling is crucial for maintaining tissue homeostasis and adapting to changing physiological demands. Disruption of this regulation contributes to numerous diseases, including osteoporosis, where impaired bone remodeling leads to bone loss and fractures [3,7]. In adipose tissue, dysregulated remodeling is linked to obesity and metabolic syndrome [6,7]. Vascular remodeling is a key process in atherosclerosis and hypertension, and its regulation by perivascular adipose tissue beiging has emerged as a novel therapeutic target. Furthermore, tissue remodeling is a hallmark of cancer progression, where tumor cells remodel their microenvironment to support growth and metastasis. Understanding the molecular mechanisms that regulate tissue remodeling is therefore essential for developing effective treatments for these conditions.
• Maintains tissue homeostasis by balancing synthesis and degradation of extracellular matrix.
• Enables adaptation to mechanical and metabolic stresses, such as weight-bearing and nutrient fluctuations.
• Regulates bone remodeling, with implications for osteoporosis and fracture healing [1,3].
• Controls adipose tissue plasticity, including beiging and thermogenesis, affecting energy balance [2,6].
• Modulates vascular remodeling, influencing blood pressure and atherosclerosis.
• Plays a role in endometrial remodeling during the menstrual cycle and pregnancy.
• Dysregulation contributes to cancer progression and metastasis.
• Circadian regulation of tissue remodeling links biological clocks to tissue health.
• Nutrient sensing pathways, such as those involving bone marrow adipose tissue, impact skeletal integrity [7,8].
• Provides targets for therapeutic intervention in metabolic and cardiovascular diseases [2,7].
What Happens During regulation of tissue remodeling?
Initiation and Sensing of Remodeling Cues
In simple terms: The body detects signals that tell it to start remodeling a tissue.
Regulation of tissue remodeling begins with the detection of physiological or pathological cues. These cues can include mechanical stress, hormonal fluctuations, circadian signals, and inflammatory cytokines [1,2]. For instance, circadian regulation of bone remodeling involves the sensing of day-night cycles by clock genes, which then modulate the activity of bone-forming osteoblasts and bone-resorbing osteoclasts. Similarly, in adipose tissue, beiging of perivascular adipose tissue is initiated by cold exposure or beta-adrenergic stimulation, leading to changes in gene expression that promote thermogenesis and vascular remodeling. Nutrient availability also serves as a critical cue; for example, weight loss affects bone marrow adipose tissue, which in turn influences skeletal remodeling.
Signal Transduction and Transcriptional Regulation
In simple terms: Signals are passed inside cells to turn genes on or off, controlling the remodeling process.
Once cues are sensed, intracellular signaling pathways transmit the information to the nucleus, where transcription factors and epigenetic regulators modulate gene expression. Epigenetic regulation of adipose tissue thermogenesis involves DNA methylation, histone modifications, and non-coding RNAs that alter the expression of thermogenic genes. In bone, circadian clock proteins interact with transcriptional regulators to control the expression of genes involved in osteoblast and osteoclast differentiation. The PNPLA3 gene, for example, is regulated in a tissue-specific manner in response to dietary and environmental challenges, affecting lipid remodeling in the liver. These transcriptional and epigenetic changes ultimately determine the rate and extent of tissue remodeling.
Effector Mechanisms: Matrix Degradation and Synthesis
In simple terms: Enzymes break down old tissue and build new tissue to reshape the organ.
The actual remodeling of tissue is carried out by effector molecules that degrade and synthesize extracellular matrix components. Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) are key regulators of this balance. In vascular remodeling, beiging of perivascular adipose tissue regulates inflammation and the activity of MMPs, thereby influencing vessel wall structure. In bone, osteoclasts secrete acid and proteases to resorb bone, while osteoblasts deposit new bone matrix [3,7]. The regulation of these effector mechanisms ensures that tissue remodeling is tightly controlled and occurs only when needed.
Integration with Systemic Metabolism
In simple terms: Tissue remodeling is connected to whole-body energy use and metabolism.
Regulation of tissue remodeling is intimately linked to systemic metabolism. Bone remodeling, for instance, is influenced by energy status and nutrient availability, with bone marrow adipose tissue acting as a sensor of weight loss and a regulator of skeletal integrity [7,8]. The role of bone in whole-body energy metabolism has been increasingly recognized, as osteocalcin and other bone-derived factors can affect glucose homeostasis and fat mass. Similarly, adipose tissue remodeling affects systemic insulin sensitivity and lipid profiles. Thus, the regulation of tissue remodeling is not an isolated process but is integrated with broader metabolic networks.
Resolution and Feedback
In simple terms: Once remodeling is done, feedback loops stop the process to prevent damage.
After tissue remodeling is completed, negative feedback mechanisms terminate the process to avoid excessive tissue degradation or deposition. For example, in bone remodeling, the coupling of bone resorption and formation ensures that the amount of bone removed is replaced, maintaining bone mass. Disruption of this feedback can lead to pathological remodeling, such as in osteoporosis where resorption outpaces formation. In adipose tissue, feedback regulation of thermogenesis prevents excessive energy expenditure. These feedback loops are critical for maintaining tissue homeostasis and preventing disease.
Key Genes Involved in GO:0034103 regulation of tissue remodeling
The following genes and proteins are key players in the regulation of tissue remodeling, as supported by published literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| CLOCK | Core circadian clock gene; regulates bone remodeling rhythm | Circadian regulation of bone remodeling |
| BMAL1 | Partner of CLOCK; controls circadian gene expression in bone | Circadian regulation of bone remodeling |
| PNPLA3 | Lipid remodeling in liver; tissue-specific regulation | Dietary and environmental challenges |
| UCP1 | Uncoupling protein 1; thermogenesis in beige adipocytes | Beiging of perivascular adipose tissue |
| PPARGC1A | Transcriptional coactivator; regulates thermogenic gene program | Epigenetic regulation of adipose thermogenesis |
| PRDM16 | Transcriptional regulator of brown/beige adipocyte differentiation | Adipose tissue thermogenesis |
| MMP2 | Matrix metalloproteinase; degrades extracellular matrix | Vascular remodeling and inflammation |
| MMP9 | Matrix metalloproteinase; involved in tissue remodeling | Vascular remodeling |
| TIMP1 | Tissue inhibitor of metalloproteinases; regulates MMP activity | Vascular remodeling |
| RANKL | Cytokine essential for osteoclast differentiation | Bone remodeling [3,7] |
| OPG | Decoy receptor for RANKL; inhibits osteoclastogenesis | Bone remodeling [3,7] |
| RUNX2 | Master transcription factor for osteoblast differentiation | Bone remodeling [1,7] |
| SP7 | Transcription factor (Osterix) for osteoblast differentiation | Bone remodeling [1,7] |
| LEPR | Leptin receptor; mediates energy status signals to bone | Nutrient regulation of bone marrow adipose tissue |
| ADIPOQ | Adiponectin; adipokine involved in metabolic regulation | Bone and energy metabolism |
| ESR1 | Estrogen receptor alpha; regulates bone remodeling | Calcium metabolism and bone health |
| VDR | Vitamin D receptor; regulates calcium and bone remodeling | Calcium metabolism |
| WNT10B | Wnt ligand; promotes osteoblastogenesis | Bone remodeling |
How Is regulation of tissue remodeling Regulated?
The regulation of tissue remodeling is controlled by a complex interplay of systemic and local factors. Circadian rhythms, mediated by core clock genes such as CLOCK and BMAL1, regulate bone remodeling by modulating the expression of genes involved in osteoblast and osteoclast activity. Nutrient availability, particularly through bone marrow adipose tissue, influences skeletal remodeling via leptin and other adipokines [7,8]. Epigenetic mechanisms, including DNA methylation and histone acetylation, regulate adipose tissue thermogenesis and beiging. In vascular tissue, beiging of perivascular adipose tissue is regulated by beta-adrenergic signaling and inflammatory cytokines, which in turn affect vascular remodeling. Additionally, tissue-specific regulation of PNPLA3 in response to dietary challenges modulates lipid remodeling in the liver. These regulatory layers ensure that tissue remodeling is appropriately timed and coordinated with physiological demands.
regulation of tissue remodeling and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| CLOCK | Circadian disruption and osteoporosis | Knockout mouse model; bone remodeling assays |
| PNPLA3 | Non-alcoholic fatty liver disease; lipid remodeling | Knock-in mouse model; liver organoids |
| UCP1 | Obesity and impaired thermogenesis | Overexpression in adipose tissue; beiging assays |
| MMP9 | Atherosclerosis and vascular remodeling | Knockout mouse; vascular injury models |
| ESR1 | Postmenopausal osteoporosis | Point mutation knock-in; bone density analysis |
Osteoporosis and Metabolic Bone Disease
Dysregulation of bone remodeling is central to osteoporosis, a disease characterized by low bone mass and increased fracture risk. Imbalances in the regulation of osteoclast and osteoblast activity, often due to hormonal changes or nutrient deficiencies, lead to excessive bone resorption [3,7]. Circadian disruption has been linked to impaired bone remodeling and bone loss. Understanding the regulatory mechanisms of bone remodeling is essential for developing therapies for osteoporosis and other metabolic bone diseases [7,8].
Cardiovascular Disease and Vascular Remodeling
Vascular remodeling is a key pathological process in atherosclerosis, hypertension, and restenosis. Beiging of perivascular adipose tissue regulates inflammation and vascular remodeling, and its dysfunction contributes to vascular disease. Matrix metalloproteinases and their inhibitors are critical effectors of vascular remodeling, and their dysregulation leads to vessel wall thickening and plaque instability. Targeting the regulation of vascular remodeling is a promising therapeutic strategy for cardiovascular disease.
Obesity and Metabolic Syndrome
Adipose tissue remodeling, including beiging and thermogenesis, is dysregulated in obesity and metabolic syndrome. Epigenetic regulation of adipose tissue thermogenesis affects energy expenditure and fat accumulation. Bone marrow adipose tissue also plays a role in whole-body energy metabolism, and its expansion during weight loss can impact skeletal health [7,8]. Thus, the regulation of tissue remodeling in adipose and bone tissues is intertwined with metabolic disease pathogenesis.
Endometrial Disorders and Cancer
Endometrial remodeling is essential for menstrual cycle progression and embryo implantation. Organoid models of endometrium have been developed to study endometrial epithelium physiology and long-term expandability, providing insights into disorders such as endometriosis and endometrial cancer. Dysregulation of tissue remodeling is also a hallmark of cancer, where tumor cells remodel the extracellular matrix to promote invasion and metastasis. Understanding the regulatory mechanisms of tissue remodeling in these contexts is critical for developing targeted therapies.
From regulation of tissue remodeling-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does gene X regulate bone remodeling in vivo? | Knockout mouse model with bone histomorphometry [1,7] |
| Does a specific point mutation in gene Y alter its function in tissue remodeling? | Point mutation knock-in mouse or cell line |
| Can overexpression of gene Z enhance tissue regeneration? | Overexpression transgenic model or viral delivery |
| What is the role of gene W in adipose tissue beiging? | Adipose-specific knockout or overexpression |
| How does gene V affect endometrial remodeling? | Endometrial organoids with CRISPR knockout |
| Does gene U mediate circadian regulation of bone remodeling? | Circadian mutant mice with bone analysis |
How to Study the regulation of tissue remodeling Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA-seq | Transcriptome changes | Identify genes differentially expressed during tissue remodeling [1,4] |
| ChIP-seq | Protein-DNA interactions and histone modifications | Map epigenetic regulation of thermogenesis |
| Proteomics | Protein abundance and modifications | Discover matrix proteins in bone remodeling |
| Metabolomics | Metabolite profiles | Assess lipid remodeling in liver |
| Micro-CT | Bone microarchitecture | Evaluate bone remodeling in knockout mice [1,7] |
| Histology | Tissue morphology | Visualize adipose beiging and vascular remodeling |
| CRISPR screen | Gene function at scale | Identify novel regulators of tissue remodeling [4,5] |
| Organoid culture | 3D tissue physiology | Study endometrial remodeling and expandability |
Genomic and Transcriptomic Approaches
RNA sequencing (RNA-seq) and single-cell RNA-seq are powerful methods to identify genes and pathways involved in the regulation of tissue remodeling. These techniques can reveal transcriptional changes in response to remodeling cues, such as circadian signals or nutrient availability [1,4]. Chromatin immunoprecipitation sequencing (ChIP-seq) can map binding sites of transcription factors and epigenetic marks, providing insights into regulatory mechanisms.
Proteomic and Metabolomic Profiling
Mass spectrometry-based proteomics and metabolomics allow the quantification of proteins and metabolites involved in tissue remodeling. For example, proteomic analysis of bone tissue can identify changes in matrix proteins and signaling molecules during remodeling. Metabolomics can reveal shifts in lipid metabolism associated with adipose tissue remodeling [4,6].
Imaging and Histological Techniques
Histology, immunohistochemistry, and advanced imaging modalities such as micro-CT and two-photon microscopy are essential for visualizing tissue architecture and remodeling processes. Micro-CT is widely used to assess bone remodeling in animal models [1,7]. Fluorescence imaging can track the beiging of adipose tissue in vivo.
Functional Genomics with CRISPR
CRISPR-Cas9 genome editing enables the creation of knockout, knock-in, and point mutation models to study gene function in tissue remodeling. Pooled CRISPR screens can identify novel regulators of remodeling processes [4,5]. These approaches are complemented by bioinformatics analyses to interpret large datasets and prioritize candidate genes.
How CRISPR Can Be Used to Study GO:0034103 regulation of tissue remodeling
Knockout
CRISPR knockout (KO) models are generated by introducing frameshift mutations in the target gene, leading to loss of function. KO models are invaluable for studying the role of specific genes in the regulation of tissue remodeling. For example, knockout of Clock or Bmal1 in mice has revealed their essential roles in circadian regulation of bone remodeling. Similarly, knockout of Pnpla3 in mice has provided insights into its tissue-specific regulation of lipid remodeling. KO cell lines and organoids can be used for mechanistic studies in vitro.
Point Mutation
Point mutation knock-in models introduce specific nucleotide changes to mimic human disease-associated variants or to dissect functional domains of a protein. For instance, point mutations in the ESR1 gene can model estrogen resistance and its impact on bone remodeling. These models are crucial for understanding how subtle genetic changes affect tissue remodeling processes and for testing targeted therapies.
Knock-in
Knock-in models allow the insertion of reporter genes, tags, or humanized sequences into a specific locus. Tagged knock-in of remodeling-related genes enables live-cell imaging and protein interaction studies. Knock-in of human PNPLA3 variants into mouse models has been used to study diet-induced lipid remodeling. These models are also used to create conditional alleles for tissue-specific studies.
Overexpression
Overexpression models drive high-level expression of a gene of interest, often using transgenic approaches or viral vectors. Overexpression of Ucp1 in adipose tissue enhances beiging and thermogenesis, affecting vascular remodeling. Overexpression of Ppargc1a in adipocytes promotes thermogenic gene programs. These models help establish sufficiency of a gene in driving tissue remodeling and can be used for gain-of-function screens.
How EDITGENE Supports regulation of tissue remodeling Research
Researchers studying regulation of tissue remodeling-related genes often need to determine whether a candidate gene is causally involved in the remodeling process. This requires precise genetic manipulation, which can be achieved through CRISPR-based genome editing. EDITGENE provides a comprehensive suite of services to support such studies, from knockout and point mutation models to overexpression and library screening.
Contact EDITGENE today to design your custom CRISPR model for regulation of tissue remodeling research.
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| GPNMB Knockout HEK293 Cell Line | EDJ-KQ2335 | Human | 10457 | Details Get a Quote |
| CST3 Knockout HEK293 Cell Line | EDJ-KQ3644 | Human | 1471 | Details Get a Quote |
| HAND2 Knockout HEK293 Cell Line | EDJ-KQ6595 | Human | 9464 | Details Get a Quote |
| THBS4 Knockout HEK293 Cell Line | EDJ-KQ14944 | Human | 7060 | Details Get a Quote |
| DDR2 Knockout HEK293 Cell Line | EDJ-KQ17791 | Human | 4921 | Details Get a Quote |
| DDR2 Knockout HCT 116 Cell Line | EDC07840 | Human | 4921 | Details Get a Quote |
| GPNMB Knockout HeLa Cell Line | EDJ-KQ21417 | Human | 10457 | Details Get a Quote |
| GPNMB Knockout A-549 Cell Line | EDJ-KQ22738 | Human | 10457 | Details Get a Quote |
| GPNMB Knockout HCT 116 Cell Line | EDJ-KQ22739 | Human | 10457 | Details Get a Quote |
| CST3 Knockout A-549 Cell Line | EDJ-KQ26881 | Human | 1471 | Details Get a Quote |
| CST3 Knockout HCT 116 Cell Line | EDJ-KQ26882 | Human | 1471 | Details Get a Quote |
| CST3 Knockout HeLa Cell Line | EDJ-KQ26883 | Human | 1471 | Details Get a Quote |
| THBS4 Knockout HCT 116 Cell Line | EDJ-KQ46635 | Human | 7060 | Details Get a Quote |
| GPNMB Knockout THP-1 Cell Line | EDJ-KZ268 | Human | 10457 | Details Get a Quote |
| DDR2 Knockout HeLa Cell Line | EDJ-KQ54033 | Human | 4921 | Details Get a Quote |
Displaying Records 1 To 15 Of 23 Records
Frequently Asked Questions About regulation of tissue remodeling
What is GO:0034103 regulation of tissue remodeling?
GO:0034103 is a Gene Ontology term defined as any process that modulates the frequency, rate, or extent of tissue remodeling. It is a biological process that encompasses the regulatory mechanisms controlling tissue reorganization.
What genes are involved in the regulation of tissue remodeling?
Key genes include CLOCK, BMAL1, PNPLA3, UCP1, PPARGC1A, PRDM16, MMP2, MMP9, TIMP1, RANKL, OPG, RUNX2, SP7, LEPR, ADIPOQ, ESR1, VDR, and WNT10B, as supported by published studies [1,2,3,4,6,7,8].
How is tissue remodeling regulated by circadian rhythms?
Circadian rhythms regulate tissue remodeling through core clock genes such as CLOCK and BMAL1, which control the timing of bone formation and resorption.
What role does adipose tissue play in vascular remodeling?
Beiging of perivascular adipose tissue regulates inflammation and vascular remodeling, influencing the structure and function of blood vessels.
How does nutrient availability affect bone remodeling?
Nutrient availability, sensed through bone marrow adipose tissue and adipokines like leptin, influences skeletal remodeling and bone mass [7,8].
What are the epigenetic mechanisms regulating adipose tissue thermogenesis?
Epigenetic mechanisms include DNA methylation, histone modifications, and non-coding RNAs that alter the expression of thermogenic genes such as UCP1.
How can CRISPR be used to study the regulation of tissue remodeling?
CRISPR can create knockout, point mutation, knock-in, and overexpression models to test the causal role of specific genes in tissue remodeling [4,5].
What diseases are associated with dysregulated tissue remodeling?
Dysregulated tissue remodeling is associated with osteoporosis, cardiovascular disease, obesity, metabolic syndrome, and cancer [2,3,6,7].
What are organoids and how are they used in tissue remodeling research?
Organoids are 3D tissue cultures that mimic organ physiology. Endometrial organoids have been developed to study endometrial epithelium physiology and long-term expandability.
How does PNPLA3 regulate lipid remodeling?
PNPLA3 is regulated in a tissue-specific manner in response to dietary and environmental challenges, affecting lipid remodeling in the liver.
Conclusion
The regulation of tissue remodeling (GO:0034103) is a critical biological process that ensures proper tissue homeostasis and adaptation. Dysregulation of this process contributes to a wide range of diseases, including osteoporosis, cardiovascular disease, and metabolic disorders. Advances in CRISPR genome editing and organoid technologies have provided powerful tools to dissect the molecular mechanisms underlying tissue remodeling regulation. Continued research in this field promises to uncover new therapeutic targets and strategies for treating diseases associated with aberrant tissue remodeling.
References
- 1. Kikyo N. 2024. Circadian Regulation of Bone Remodeling.. Int J Mol Sci 25(9) PMID: 38731934
- 2. Adachi Y et al.. 2022. Beiging of perivascular adipose tissue regulates its inflammation and vascular remodeling.. Nat Commun 13(1):5117 PMID: 36071032
- 3. Peacock M. 2010. Calcium metabolism in health and disease.. Clin J Am Soc Nephrol 5 Suppl 1:S23-30 PMID: 20089499
- 4. Wu P et al.. 2026. Tissue-specific regulation of PNPLA3 promotes lipid remodeling in response to dietary and environmental challenges.. J Hepatol 85(1):48-60 PMID: 41802497
- 5. Boretto M et al.. 2017. Development of organoids from mouse and human endometrium showing endometrial epithelium physiology and long-term expandability.. Development 144(10):1775-1786 PMID: 28442471
- 6. Zhao QW et al.. 2022. Progress on the epigenetic regulation of adipose tissue thermogenesis.. Yi Chuan 44(10):867-880 PMID: 36384724
- 7. Rosen CJ et al.. 2023. Nutrient regulation of bone marrow adipose tissue: skeletal implications of weight loss.. Nat Rev Endocrinol 19(11):626-638 PMID: 37587198
- 8. Lecka-Czernik B et al.. 2025. The role of bone in whole-body energy metabolism.. Nat Rev Endocrinol 21(12):743-756 PMID: 40846895
