Humanin

HN and MOTS-c were significantly downregulated in human AF atrial tissue and inversely correlated with fibrosis extent.; Plasma MOTS-c was decreased in AF patients and inversely correlated with NT-proBNP.; HNG or MOTS-c treatment reduced AF inducibility and attenuated AngII-induced atrial fibrosis and hypertrophy in mice.; Peptide treatment improved mitochondrial ultrastructure, reduced fission proteins (Drp1, Fis1), and lowered pro-inflammatory cytokines (IL-1, IL-6).

MDPs, including humanin, MOTS-c, and SHLPs, show promise for treating AD, PD, and HD.; MDPs mitigate Amyloid-beta toxicity in AD, dopaminergic neuron loss in PD, and mutant huntingtin aggregation in HD.; MDPs attenuate oxidative stress and neuroinflammation in neurodegenerative models.; Current research lacks precise molecular pathway understanding, targeted delivery methods, and clinical translation.

HN and MOTS-c transcript levels differed significantly among AD, MCI, and SCD groups; Blood and plasma transcript levels of these peptides were significantly reduced in AD compared to SCD; Plasma HN and MOTS-c protein concentrations did not discriminate between AD and MCI; In silico and RNA decay assays showed faster degradation of HN mRNA and delayed but stable recovery of MOTS-c mRNA

PD pathogenesis is complex, involving mitochondrial dysfunction, oxidative stress, neuroinflammation, impaired autophagy, and ER-Golgi stress, alongside alpha-synuclein aggregation and Lewy body formation.; Mitochondrial dysfunction is of special interest due to its key role in energy metabolism and ROS generation that can hasten neuronal damage.; MDPs including Humanin, SHLPs, and MOTS-c have been identified as modulators of cellular stress responses.; MDPs may impact major PD pathogenic processes such as inflammation, oxidative stress, and metabolic dysfunction, making them candidate targets for disease-modifying therapies.

Human efferocytic macrophages show common modulation of mitochondrial metabolism-related genes, including PLIN5 and MTLN.; HUMANIN (MT-RNR2) is produced early during resolution of inflammation in a mouse peritonitis model.; Preventive HUMANIN administration reduces leukocyte infiltration and pro-inflammatory cytokines in mice.; HUMANIN dampens pro-inflammatory cytokine secretion in primary human neutrophils and is detected in human periodontitis gingival fluid.

Humanin and GAS5 were significantly downregulated in precancerous lesions and prostate cancer compared to benign prostatic hyperplasia.; Exosomal miR-21 showed outstanding discriminative power between BPH and precancerous lesions (AUC = 1.000) and between precancerous lesions and prostate cancer (AUC = 0.9932).; MOTS-c levels were elevated in precancerous lesions compared to BPH, suggesting involvement in early malignant transformation.; A plasma-only model combining Humanin, GAS5, and MOTS-c achieved 95% cross-validated classification accuracy across clinical groups.

Male IUGR offspring exposed to HFhf showed greater metabolic dysfunction (adiposity, glucose intolerance, insulin resistance, hyperlipidemia, hepatomegaly with steatosis) than females.; Hepatic gene expression diverged by sex: males upregulated triglyceride synthesis and de novo lipogenesis genes, while females upregulated lipolysis, β-oxidation, fatty acid efflux, and FGF21 genes.; IUGR-HFhf males had reduced pancreatic islet insulin and humanin; humanin suppression impaired glucose-stimulated insulin secretion, ATP production, and islet viability.; Humanin and FGF21 may reverse the perinatal nutritional mismatch phenotype by restoring functional islets and preventing MASLD and diabetes mellitus.

HN expression is downregulated in IDD patients, and this is corroborated in cell and rat IDD models.; Exogenous HN triggers endogenous HN expression and impedes JAK2/STAT3 and NF-κB pathways, mitigating erastin-induced ferroptosis in NP cells, dependent on HSP27 upregulation.; HN preserves mitochondrial homeostasis, curbing mtROS generation and mtDNA leakage, thereby hindering mtDNA-TLR9 binding and NF-κB pathway activation.; In vivo, HN treatment ameliorates IDD progression induced by annulus fibrosus puncture in rats.

What is Humanin?

**Mechanism of Action** Humanin (HN) is a 24-amino acid mitochondrial-derived peptide that exerts cytoprotective effects primarily through binding to a heterotrimeric receptor complex comprising ciliary neurotrophic factor receptor α (CNTFR), gp130, and WSX-1. This interaction activates downstream signaling pathways, i

How does Humanin work?

Mitochondrial-derived 24-aa peptide with cytoprotective, anti-apoptotic, and insulin-sensitizing effects in aging and neurodegeneration models.

What is the research status of Humanin?

Humanin is currently classified as preclinical, with 550 research references on record. This is for research purposes only and is not medical advice.

What is the molecular weight of Humanin?

Humanin has a molecular weight of approximately 2687.2 g/mol (formula C119H204N34O32S2).