Molecular Mechanisms of Development and Reversal of Alcohol Induced Liver Fibrosis (R01) | Apply Online

Opportunity Summary:

The National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health (NIH), issued this Funding Opportunity Announcement (FOA) to support research that explains, at a molecular level, how alcohol use drives liver fibrosis and how that fibrotic process might be reversed. The core scientific focus is on alcoholic liver fibrosis as a biologic process characterized by the excessive buildup of extracellular matrix (ECM) material, especially collagen, which disrupts normal liver architecture and function. A major emphasis of the announcement is the central role of hepatic stellate cells (HSCs): once activated, these cells become key producers of collagen and other ECM components, making HSC activation a critical trigger and sustaining event in fibrogenesis. By funding studies that clarify these pathways, NIAAA is aiming to accelerate the development of better preventive and therapeutic strategies for alcohol-induced liver disease.

The FOA specifically invites R01 applications proposing mechanistic studies of both development and reversal of fibrosis, not just descriptive work. In practical terms, applicants are expected to dig into the signaling pathways, gene regulation, cellular interactions, and molecular drivers that turn alcohol exposure into progressive scarring, and to identify what biologic switches might allow the liver to move back toward normal structure once injury is reduced or treatment is applied. A notable feature is the encouragement to test small molecules that could prevent fibrosis from forming or actively reverse established fibrosis. That means the opportunity is open to work that moves beyond mapping pathways and into evaluating targeted compounds, provided the science remains grounded in mechanisms and uses rigorous experimental designs.

This opportunity uses the NIH Research Project Grant (R01) mechanism, which typically supports more mature, hypothesis-driven projects with a broader scope than exploratory awards. The FOA is paired with a parallel announcement of the same scientific scope using the R21 mechanism (PA-07-361), which is generally geared toward earlier-stage or higher-risk exploratory studies. Applicants choosing the R01 route are therefore positioning their work as sufficiently developed to justify a full research project grant structure, including more extensive aims, validation, and potentially translational components such as therapeutic testing in relevant models.

Funding levels and the number of awards are not fixed. Awards are contingent on the availability of appropriated funds and on how many high-quality, meritorious applications are submitted. Because proposed projects may vary widely in approach, model systems, and experimental breadth, the FOA notes that both award size and project duration will vary accordingly. In other words, the institute is leaving room for different scales of research plans, and final totals will depend on the mix of application budgets, timelines, and scientific merit.

Eligibility is broad and includes many types of organizations. Eligible applicants include public and state-controlled institutions of higher education, private institutions of higher education, state governments, small businesses, other for-profit organizations that are not small businesses, nonprofits (including those with 501(c)(3) status as well as certain nonprofits without 501(c)(3) status), and other applicant types as allowed under NIH policy. Importantly, foreign institutions are also eligible to apply, which can support international collaborations or allow non-U.S. institutions with relevant expertise and resources to compete directly. There is no cost sharing or matching requirement, aligning with typical NIH research grant practices.

Administratively, the opportunity is identified as PA-07-360, categorized as discretionary grant funding within the health activity area, and associated with CFDA number 93.273 (Alcohol Research Programs). The posting date is listed as April 19, 2007, with multiple receipt dates rather than a single deadline, meaning applications could be accepted on standard NIH submission cycles while the announcement remained active. The archived date is April 5, 2010, indicating the FOA is no longer active, though it remains useful as a reference for the type of projects NIAAA has sought to fund in this area.

At a high level, the announcement is designed for investigators who can connect alcohol exposure to the molecular events that activate stellate cells, drive collagen-rich ECM accumulation, and shape the balance between progressive scarring and potential regression. Competitive applications under this FOA would be expected to clearly define the molecular targets and pathways involved, use strong experimental models and analytic methods to establish causality, and, where relevant, provide a credible plan for testing small molecules that could realistically prevent or reverse alcohol-induced fibrotic changes.

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Next opportunity: Molecular Mechanisms of Development and Reversal of Alcohol Induced Liver Fibrosis (R21)

Previous opportunity: Collaborative Neurological Sciences (CNS) Award (S11)

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