Digital PNG artwork · delivered by email | Secure checkout · no physical shipping
Hedi Raizer

Journal 5 min read

Which peptides are studied in relation to autophagy?

A research-supply overview of peptides and related compounds investigated in autophagy studies, spanning in vitro, animal, and clinical models. For laboratory research use only.

peptides-pro Editorial

Which peptides are studied in relation to autophagy?

Peptides and small molecules investigated in autophagy research include ATG13, a component of the autophagy initiation complex; fisetin, a flavonoid; astaxanthin, a carotenoid; and hepassocin (HPS), a hepatokine. These agents are examined in models such as influenza A virus infection, Alzheimer's disease neurotoxicity, polyendocrine metabolic ovarian syndrome (PMOS), and liver aging. Identifiers such as sequence, formula, or molecular weight are not provided in the evidence for these compounds.

The work centres on the autophagy-lysosomal pathway and its regulation by upstream kinases and ubiquitin-like conjugation systems.

Research Studies

ATG13 and influenza A virus restriction via MAVS ubiquitination

ATG13 is an autophagy-associated protein that regulates the assembly of the autophagy initiation complex. In the context of influenza A virus (IAV) infection, ATG13 restricts viral replication while potentiating type I interferon (IFN-I) signalling. Mechanistically, ATG13 interacts with MAVS and recruits the E3 ubiquitin ligase ASB1 to catalyse K63-linked polyubiquitination at the K348 residue of MAVS, amplifying antiviral signalling [2]. This study was conducted in vitro and in cell-based assays.

Fisetin and amyloid-beta-induced neurotoxicity in SH-SY5Y cells

Fisetin, a natural flavonoid, was evaluated for neuroprotective effects using in silico methods and an Aβ1-42-induced neurotoxicity model in human neuroblastoma SH-SY5Y cells. In silico studies indicated that fisetin binds strongly and stably to ULK1 (an autophagy marker), p21 (a senescence/cell cycle marker), and synaptophysin (a synaptic marker) [7]. This evidence is in vitro and in silico only.

Astaxanthin and granulosa cell autophagy in PMOS-associated infertility

A triple-blind, placebo-controlled pilot randomised trial investigated whether astaxanthin (AST) modulates autophagy-related signalling in granulosa cells (GCs) from women with polyendocrine metabolic ovarian syndrome (PMOS)-related anovulatory infertility. Fifty women received AST (12 mg/day) or placebo, and the study assessed autophagy-related signalling and ovarian response [6]. This is clinical evidence in a specific patient population.

Hepassocin and age-related liver senescence via AMPK activation

Hepassocin (HPS), a hepatokine, was studied for its role in preventing age-related liver senescence and facilitating liver regeneration by activating AMPK [10]. This finding is from animal or in vitro models, as detailed in the reference.

LSD1 and DNA damage-mediated senescence and organ aging

LSD1 (lysine-specific demethylase 1) was found to interact with and demethylate ATM at lysine 3,016, sustaining ATM phosphorylation and amplifying DNA damage signalling, thereby promoting senescence and organ aging. This was observed in aged organs and senescent cells, and in response to ionizing radiation-induced DNA damage [3]. The evidence is from animal and cellular models.

Autophagy in hypothalamic POMC and AgRP neurons and obesity

In the arcuate nucleus, autophagy exerts divergent metabolic effects in the two principal appetite-regulating neuronal populations, POMC and AgRP neurons, with implications for obesity [9]. This is a reference-only finding from a review or study, and the specific mechanisms are not detailed here.

Radiation-induced atrial fibrillation and senolytic therapy

Radiation-induced atrial fibrillation is driven by cellular senescence via the GATA4-NF-κB pathway and can be rescued by D/Q senolytic therapy [11]. This finding is from an animal model of radiation-induced heart disease.

Prevotella intermedia and alveolar macrophage function

Prevotella intermedia culture supernatant impairs alveolar macrophage function and promotes Mycobacterium avium persistence [12]. This is a reference-only finding from in vitro or ex vivo studies.

Fasting, exercise, and diet to activate autophagy in depression

A clinical trial is investigating how lifestyle factors such as physical activity and diet-related processes may influence autophagy, a natural cellular process that helps cells remove damaged components, in the context of depression [5]. This is an ongoing clinical study.

Inorganic phosphate and exercise intolerance

Chronic inorganic phosphate (Pi) excess from ultra-processed foods may impair skeletal muscle energetics and contribute to exercise intolerance, with potential links to autophagy [8]. This evidence is from observational and mechanistic studies in humans and animal models.

Astrocytic failure in Parkinson's disease

In Parkinson's disease, pathological α-synuclein triggers astrocytic failure, including impaired proteostasis via ubiquitin-proteasome and autophagy-lysosomal pathways, glymphatic system collapse due to aquaporin-4 (AQP4) depolarization, and chronic neuroinflammation [1]. This is a system-level model based on review of multiple studies.

If you are reading this for personal health reasons

The compounds mentioned here are sold for laboratory research use only. We do not provide dosing or medical guidance. Anyone considering a compound for themselves should speak to a licensed clinician.

Sources

WhatsApp