Exploring the therapeutic potential of lupeol: A review of its mechanisms, clinical applications, and advances in bioavailability enhancement.

Lupeol, a naturally occurring triterpenoid, has garnered significant attention for its diverse range of biological activities and potential therapeutic applications. This comprehensive review delves into the various aspects of lupeol, including its sources, extraction methods, chemical characteristics, pharmacokinetics, safety evaluation, mechanisms of action, and applications in disease treatment. We highlight the compound's unique carbon skeleton and its role in inflammation regulation, antioxidant activity, and broad-spectrum antimicrobial effects.

Bioactive components, pharmacological properties and underlying mechanism of spore oil: A review.

is a Chinese medicinal fungus with a long history of use in healthcare and disease treatment. spores (GLS) are tiny germ cells released from the mushroom cap during the mature stage of growth. They contain all the genetic active substances of .

Unveiling OSCP as the potential therapeutic target for mitochondrial dysfunction-related diseases.

Mitochondria are important organelles in cells responsible for energy production and regulation. Mitochondrial dysfunction has been implicated in the pathogenesis of many diseases. Oligomycin sensitivity-conferring protein (OSCP), a component of the inner mitochondrial membrane, has been studied for a long time.

A new direction in Chinese herbal medicine ameliorates for type 2 diabetes mellitus: Focus on the potential of mitochondrial respiratory chain complexes.

Ethnopharmacological Relevance: Diabetes is a common chronic disease. Chinese herbal medicine (CHM) has a history of several thousand years in the treatment of diabetes, and active components with hypoglycemic effects extracted from various CHM, such as polysaccharides, flavonoids, terpenes, and steroidal saponins, have been widely used in the treatment of diabetes.

Aim Of The Study: Research exploring the potential of various CHM compounds to regulate the mitochondrial respiratory chain complex to improve type 2 diabetes mellitus (T2DM).

ATP synthase inhibitory factor subunit 1 regulates islet β-cell function via repression of mitochondrial homeostasis.

Mitochondrial homeostasis is crucial for the function of pancreatic β-cells. ATP synthase inhibitory factor subunit 1 (IF1) is a mitochondrial protein interacting with ATP synthase to inhibit its enzyme activity. IF1 may also play a role in maintaining ATP synthase oligomerization and mitochondrial inner membrane formation.

ATPAF1 deficiency impairs ATP synthase assembly and mitochondrial respiration.

ATP11p and ATP12p are two nuclear-encoded mitochondrial chaperone proteins required for assembling the F1Fo-ATP synthase F1 sector. ATPAF1 and ATPAF2 are the mammalian homologs of ATP11p and ATP12p. However, the biochemical and physiological relevance of ATPAF1 and ATPAF2 in animal tissues with high energy-dependence remains unclear.

San1 deficiency leads to cardiomyopathy due to excessive R-loop-associated DNA damage and cardiomyocyte hypoplasia.

R-loops are naturally occurring transcriptional intermediates containing RNA/DNA hybrids. Excessive R-loops cause genomic instability, DNA damage, and replication stress. Senataxin-associated exonuclease (San1) is a protein that interacts with Senataxin (SETX), a helicase resolving R-loops.

Mitochondrial respiration in C57BL/6 substrains varies in response to myocardial infarction.

The C57BL/6 mouse strain have been commonly used for the genetic background animal models and experimental research. There are several major sources of C57BL/6 substrains for the biomedical research community which display genetic and phenotypic differences. Previous studies have suggested that the varies in baseline of cardiovascular phenotypes as well as in response to pressure overload by transverse aortic constriction (TAC).

Sustained Oligomycin Sensitivity Conferring Protein Expression in Cardiomyocytes Protects Against Cardiac hypertrophy Induced by Pressure Overload via Improving Mitochondrial Function.

Cardiac hypertrophy is a major risk factor for congestive heart failure, a leading cause of morbidity and mortality. Abrogating hypertrophic progression is a well-recognized therapeutic goal. Mitochondrial dysfunction is a hallmark of numerous human diseases, including cardiac hypertrophy and heart failure.

Assessing Mitochondrial Bioenergetics in Isolated Mitochondria from Mouse Heart Tissues Using Oroboros 2k-Oxygraph.

In this chapter, we describe detailed protocols for measuring high-resolution respirometry on mitochondria extracted from adult whole mouse heart using the Oroboros 2k-Oxygraph system. The method provides detailed procedures for the preparation of mitochondria and measurement of high-resolution respirometry in response to various respiration inhibitions. The method described in this chapter could discern the different respiration rate on mitochondria extracted from two spatially distinct mitochondrial subpopulations, subsarcolemmal mitochondria (SSM) and intermyofibrillar mitochondria (IFM).

PPAR, a Potential Therapeutic Target for Heart Disease.

The nuclear receptor peroxisome proliferator-activated receptor (PPAR) can transcriptionally regulate target genes. PPAR exerts essential regulatory functions in the heart, which requires constant energy supply. PPAR plays a key role in energy metabolism, controlling not only fatty acid (FA) and glucose oxidation, but also redox homeostasis, mitochondrial biogenesis, inflammation, and cardiomyocyte proliferation.

Honokiol protects against doxorubicin cardiotoxicity via improving mitochondrial function in mouse hearts.

Honokiol is a key component of a medicinal herb, Magnolia bark. Honokiol possesses potential pharmacological benefits for many disease conditions, especially cancer. Recent studies demonstrate that Honokiol exerts beneficial effects on cardiac hypertrophy and doxorubicin (Dox)-cardiotoxicity via deacetylation of mitochondrial proteins.

Knockout of the ATPase inhibitory factor 1 protects the heart from pressure overload-induced cardiac hypertrophy.

Mitochondrial ATP synthase catalyzes the coupling of oxidative phosphorylation. Under pathological conditions, ATP synthase hydrolyzes ATP to replenish protons from the matrix into the intermembrane space, sustaining mitochondrial membrane potential. ATPase inhibitory factor 1 (IF1) is a nuclear-encoded, ATP synthase-interacting protein that selectively inhibits the hydrolysis activity of ATP synthase, which may render the protective role of IF1 in ischemic hearts.

Live cell screening platform identifies PPARδ as a regulator of cardiomyocyte proliferation and cardiac repair.

Zebrafish can efficiently regenerate their heart through cardiomyocyte proliferation. In contrast, mammalian cardiomyocytes stop proliferating shortly after birth, limiting the regenerative capacity of the postnatal mammalian heart. Therefore, if the endogenous potential of postnatal cardiomyocyte proliferation could be enhanced, it could offer a promising future therapy for heart failure patients.

Regulation of mitochondrial ATP synthase in cardiac pathophysiology.

Mitochondrial function is paramount to energy homeostasis, metabolism, signaling, and apoptosis in cells. Mitochondrial complex V (ATP synthase), a molecular motor, is the ultimate ATP generator and a key determinant of mitochondrial function. ATP synthase catalyzes the final coupling step of oxidative phosphorylation to supply energy in the form of ATP.

Carnitine Palmitoyltransferase 1b Deficiency Protects Mice from Diet-Induced Insulin Resistance.

Background: Carnitine Palmitoyl Transferase 1 (CPT1) is the rate-limiting enzyme governing long-chain fatty acid entry into mitochondria. CPT1 inhibitors have been developed and exhibited beneficial effects against type II diabetes in short-term preclinical animal studies. However, the long-term effects of treatment remain unclear and potential non-specific effects of these CPT1 inhibitors hamper in-depth understanding of the potential molecular mechanisms involved.

Adipose induces myoblast differentiation and mediates TNFα-regulated myogenesis.

Skeletal muscle formation is controlled by multiple processes. These processes are tightly regulated by muscle regulatory factors. Genes that are highly and specifically expressed during myogenesis need to be identified.

Molecular cloning and characterization of the anti-obesity gene adipose in pig.

Obesity has become an epidemic health problem characterized by aberrant energy metabolism. As the major player in energy homeostasis, adipose tissue has a decisive role in the development of obesity. Many genes involved in adipogenesis are also correlated with obesity.

Carnitine palmitoyltransferase-1b deficiency aggravates pressure overload-induced cardiac hypertrophy caused by lipotoxicity.

Background: Carnitine palmitoyltransferase-1 (CPT1) is a rate-limiting step of mitochondrial β-oxidation by controlling the mitochondrial uptake of long-chain acyl-CoAs. The muscle isoform, CPT1b, is the predominant isoform expressed in the heart. It has been suggested that inhibiting CPT1 activity by specific CPT1 inhibitors exerts protective effects against cardiac hypertrophy and heart failure.

Molecular cloning and characterization of the porcine Ero1L and ERp44 genes: potential roles in controlling energy metabolism.

Disulfide bond formation is a pivotal step in the maturation and release of secretory proteins that is controlled by specific endoplasmic reticulum (ER) resident enzymes. An important element in this process is Ero (ER oxidoreduction), a glycosylated flavoenzyme tightly associated with oxidative protein folding that lacks the known ER retention motifs. ER resident protein 44kDa (ERp44) is an ER resident protein that mediates ERo1 localization in ER and also prevents the secretion of unassembled cargo proteins with unpaired cysteine.

Peroxisome proliferator-activated receptor-gamma increases adiponectin secretion via transcriptional repression of endoplasmic reticulum chaperone protein ERp44.

Adiponectin, an adipocyte-derived hormone, is a versatile player involved in the regulation of energy homeostasis, cardiovascular disease, and diabetes. Within adipocytes, adiponectin is retained in the lumen of the endoplasmic reticulum (ER) by binding to the thiol protein ER resident protein 44 kDa (ERp44), which is apparently regulated by the activation of nuclear receptor peroxisome proliferator-activated receptor (PPAR)-gamma. However, the precise role of ERp44 in adiponectin secretion remains elusive.

Porcine KLF gene family: Structure, mapping, and phylogenetic analysis.

The Kruppel-like factors (KLFs) belong to the family of zinc finger-containing transcription factors that regulates a diverse array of cellular processes, including cell proliferation, differentiation, and apoptosis. Here we reported the structure, mapping and phylogenetic analysis of KLF gene family in pigs. Comparative analyses revealed strong conservation between pig and human KLFs at the genomic and protein structure levels.

Lipid accumulation mediated by adiponectin in C2C12 myogenesis.

Plasma concentrations of adiponectin have been shown to be decreased in patients with obesity, cardiovascular diseases, hypertension and metabolic syndrome. Recent studies have found that adiponectin reduces lipid accumulation in macrophage foam cells which may impact the development of atherosclerosis. However, it remains unclear whether adiponectin is involved in the process of lipid accumulation during myogenesis.

Arachidonic acid induces acetyl-CoA carboxylase 1 expression via activation of CREB1.

Acetyl-CoA carboxylase (ACC; EC 6.4.1.